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Severe mental health and metabolic symptoms may be ameliorated by a ketogenic diet.

Severe mental health and metabolic symptoms may be ameliorated by a ketogenic diet.

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In the United States, mental health disorders are thought to impact at least 578 million adults. Included in this are serious illnesses like schizophrenia and bipolar disorder. Antipsychotic drugs are sometimes necessary for the treatment of symptoms, but they can also have detrimental effects on metabolism, including weight gain and insulin resistance, which can make people feel worse about themselves and sometimes force them to stop taking their medications. To address these issues, Stanford Medicine recently conducted a pilot study to determine whether a ketogenic diet could improve the metabolic and psychiatric outcomes of patients with severe mental illness.

Diabetes, obesity, and mental health issues are just a few of the conditions that have been successfully managed by the ketogenic diet, which is high in fats, low in carbs, and moderate in protein. A 4-month ketogenic diet intervention may now dramatically improve symptoms and quality of life in individuals with severe mental illness and metabolic conditions when combined with standard medication and treatment, according to a pilot study from Stanford Medicine.

According to recent research, following a ketogenic diet that consists of high-fat, low-carb foods may help reduce weight gain and other side effects from the medications used to treat serious mental illness. Researchers at Stanford Medicine conducted a clinical trial in which they enrolled 23 patients with bipolar disorder or schizophrenia and gave them dietary instructions to consume roughly 60% fat, 30% protein, and 10% carbohydrates. Researchers have found that drugs used to treat severe mental illness can have “major metabolic side effects,” like weight gain and insulin resistance. All of the patients in the study experienced at least one of these symptoms. Upon completing a four-month ketogenic diet, a significant improvement in psychiatric symptoms was observed in 79% of the participants.

Further research is required to ascertain whether dietary modifications can significantly, long-term benefit patients with schizophrenia or bipolar disorder, given the small size and brief duration of the study. However, the results are part of an expanding body of evidence pointing to a strong connection between diet and brain health. Additionally, studies on the ketogenic diet have been conducted to treat epilepsy and Alzheimer’s disease. Theoretically, by addressing metabolic problems, the diet may lessen mental symptoms. The working theory, according to study lead author Shebani Sethi, a clinical associate professor of psychiatry and behavioral sciences at Stanford Medicine, is that we’re giving the brain energy to get around these metabolic deficiencies.

Researchers are aware that a ketogenic diet can help the brain, but Sethi said it is still unclear how much the diet can specifically help with schizophrenia or bipolar disorder. Initial search strategies turned up a total of 32 experimental or observational studies, 14 of which satisfied the requirements to be included in this analysis. While the exact diet plans used in each study varied slightly, they all primarily looked at low-carb dietary intake to induce a ketotic state. According to the studies in this review, KD helped lower symptoms related to a range of psychiatric conditions.

There are various theories regarding the application of KD to treat mental health disorders. The γ-aminobutyric acid (GABA) to glutamate ratio in the brain is thought to be altered by the KD, favoring GABA. Theoretically, the imbalanced GABA levels in a person with schizophrenia could be compensated for by this increase in GABA, which would then lessen symptoms like delusions and hallucinations.

Additionally, it is believed that ketogenic diets reduce reactive oxygen species and raise levels of phosphocreatine, adenosine triphosphate, and other nutrients that enhance metabolic efficiency. This may be advantageous for people on medications that increase their risk of gaining weight. This may lessen brain inflammation, which could relieve symptoms in a variety of illness states, including Alzheimer’s disease. 7 There is also another theory that suggests ketosis limits neuronal excitability and apoptosis, which could account for the positive reports of KD in epileptic patients.

Due to beneficial changes in the gut microbiome, the metabolic alterations linked to seizure reduction may also have potential benefits in individuals with autism spectrum disorder (ASD). Acidic plasma is thought to stabilize mood in bipolar disorder by decreasing intracellular calcium and sodium. The KD improves daytime sleepiness by increasing the activation of orexin-containing neurons in narcolepsy patients by causing relative hypoglycemia. This systematic review aims to investigate the clinical effects of KD on different states of psychiatric illness. The examined research offers proof that the KD may help treat schizophrenia, bipolar disorder, ASD, Alzheimer’s disease, and anorexia nervosa.

REFERENCES:
https://www.washingtonpost.com/wellness/2024/04/02/ketogenic-bipolar-mental-diet/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8120987/
https://www.medicalnewstoday.com/articles/a-keto-diet-may-help-improve-severe-mental-health-metabolic-symptoms

Medications that have been suggested by doctors worldwide are available here
https://mygenericpharmacy.com/index.php?cPath=77_478

Researchers discover new protein connected to dementia with early onset.

Researchers discover new protein connected to dementia with early onset.

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Researchers at the Medical Research Council (MRC) Laboratory of Molecular Biology in Cambridge, UK, have disproved earlier theories regarding frontotemporal dementia by discovering a novel protein called TAF15 that forms aggregated structures in cases of the illness. This finding adds something new to the small list of proteins known to aggregate in neurodegenerative diseases such as Alzheimer’s. This discovery not only opens the door to more sophisticated diagnostic methods and therapeutic approaches, but it also raises the intriguing possibility that TAF15 is connected to both motor neuron disease and frontotemporal dementia, providing new insights into these crippling conditions. The majority of neurodegenerative diseases, including dementia, are caused by proteins that aggregate into filaments called amyloids. Most of the time, researchers have identified the specific proteins that cause this aggregation, which allows them to concentrate on these proteins for diagnostic evaluations and treatment planning. Nevertheless, the precise protein causing frontotemporal dementia has not yet been identified by researchers in about 10% of cases. Researchers have now successfully determined the TAF15 protein’s aggregated structures in these specific instances.

The brain’s frontal and temporal lobes, which control emotions, personality, behavior, language comprehension, and speech, begin to degenerate with frontotemporal dementia. Compared to Alzheimer’s disease, this disorder usually shows symptoms earlier in life and is often diagnosed in people between the ages of 45 and 65. That can, however, also manifest in people of all ages. Scientists have discovered aggregated protein structures in their latest work, which could be a central point for future developments in diagnostic evaluations and treatments. Now that the essential protein and its structure have been found, scientists can concentrate on using it to identify and treat this particular type of frontotemporal dementia. This strategy is similar to those that are currently being used to target tau and amyloid-beta protein aggregates, which are characteristic characteristics of Alzheimer’s disease. The researchers examined protein aggregates in the brains of four patients suffering from this type of frontotemporal dementia at the atomic level resolution using sophisticated cryo-electron microscopy (cryo-EM) techniques. Up until now, researchers have linked this kind of dementia to other neurodegenerative illnesses and believed that a protein called FUS was in charge of aggregation.

The MRC Laboratory of Molecular Biology researchers were able to ascertain that the protein aggregates present in every brain had the same atomic structure by employing cryo-electron microscopy (cryo-EM). Remarkably, TAF15, a different protein, rather than FUS, was the guilty party. The researchers explained that this result was unexpected because, up until this study, neither the structural properties of TAF15 nor its involvement in the formation of amyloid filaments in neurodegenerative conditions had been identified. Through insights that were previously unattainable with earlier technologies, cryo-EM is revolutionizing our understanding of the molecular mechanisms underlying dementia and neurodegenerative diseases in a broader context. The complexity of cryo-electron microscopy, the researchers admitted, restricted their analysis to the brains of just four people. However, there is a chance that we will be able to develop instruments for screening hundreds of patient samples in order to determine the degree of these aberrant protein aggregates, now that we have a better understanding of the pivotal protein and its structure. A progressive loss of muscle control is a characteristic of motor neuron disease, which is also experienced by some people with frontotemporal dementia. In this study, two people with both conditions gave their brains for examination.

In these instances, the TAF15 protein was found in aggregated form in brain areas linked to motor neuron disease, according to the researchers. It is possible that TAF15 plays a role in the development of both frontotemporal dementia and motor neuron disease because two people who had both conditions had identical TAF15 aggregates. The investigators are currently investigating whether patients with motor neuron disease who do not show frontotemporal dementia symptoms have these aberrant TAF15 aggregates. This study further examined the possibility that additional abnormal proteins may be contributory to the neuropathological process of fronto temporal lobar degeneration and dementia (FTLD), stated James Giordano, PhD, MPhil, Pellegrino Center Professor of Neurology and Biochemistry at Georgetown University Medical Center. Giordano was not involved in this research and told Medical News Today. The investigation, which was well-conducted, examined the presence and amount of TAF protein, a variant abnormal protein constituent. TAF protein, along with other known abnormal proteins (like characteristic tau and alpha-synuclein entities), are found in and contribute to the neurodegenerative processes of frontotemporal dementia (FTLD). Dr. According to Giordano, this study importantly demonstrated that TAF protein is also present in the total proteinopathic constituency of the, albeit at a somewhat lesser concentration.

The results of the study further support and advance aspects of the amyloid hypothesis of neurodegenerative dementia, according to Dr. Giordano. He added that the discovery of the TAF variant might be a useful diagnostic marker in addition to a possible therapeutic target for the management of FTLD. Jennifer Bramen, M.D. D. Frontotemporal lobe dementia (FTD) is an emotionally taxing illness for which there is no known treatment, according to a senior research scientist at the Pacific Neuroscience Institute in Santa Monica, California, who was not involved in this study. Dr. Bramen came to the conclusion that FTD is a heterogeneous disease, which makes research on it more difficult. Increased patient treatment options may result from a deeper comprehension of various subtypes.

REFERENCES:

https://www.medicalnewstoday.com/articles/scientists-find-new-protein-linked-early-onset-dementia
https://www.sciencedaily.com/releases/2023/12/231206115845.htm
https://www.mcknights.com/news/clinical-news/scientists-identify-protein-linked-to-early-onset-dementia/
https://www.sciencealert.com/unexpected-protein-linked-to-early-onset-dementia-in-huge-discovery

For mental health medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

Supplements containing cocoa extract have been shown to improve older adults’ cognitive function.

Supplements containing cocoa extract have been shown to improve older adults’ cognitive function.

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According to a recent randomized controlled trial, older adults who eat a poor-quality diet may benefit cognitively from taking daily supplements of cocoa extract. The authors found that older adults who regularly ate a high-quality diet showed no cognitive benefit from cocoa extract. Flavanols, which are abundant in cocoa, may reduce inflammation and oxidative stress. There is still need for more investigation into the possible cognitive advantages of cocoa. According to a recent study, older adults with routinely poor diet quality may benefit cognitively from taking daily cocoa extracts. Daily doses of cocoa extract did not appear to improve cognitive function in any of the study participants. The authors of the study note a borderline trend for people with inadequate diets, though. The COcoa Supplement and Multivitamin Outcomes Study (COSMOS), a randomized clinical trial (RCT) carried out at Brigham and Women’s Hospital in Boston, Massachusetts, comprised the clinical cohort of participants in this study. The benefits of taking a daily multivitamin-mineral supplement for cancer prevention and a daily cocoa extract supplement for cognitive function were examined in this larger trial, which involved 21,442 older Americans.

A portion of the research’s funding came from Mars Edge, an entity under Mars Inc. committed to the study of nutrition. Among the other donors were the U. S. The FDA, Pfizer Consumer Healthcare, Harvard Catalyst, Contract Pharmacal Corp., and the National Institutes of Health. The American Journal of Clinical Nutrition publishes the findings. The authors claim that there has been inconsistent research on the impact of cocoa on cognitive health. The small effect observed in this study for individuals with poor diet quality points to a need for more investigation. There were 573 older participants in the study, with a mean age of 69.6. Women made up 49.2 percent of this group. At the start of the study, each participant received a thorough cognitive evaluation, and over the following two years, they underwent follow-up testing. A daily supplement containing 500 mg of cocoa extract, which included 80 mg of the antioxidant epicatechin, was given to certain study participants, while control participants were given a placebo. A total of 492 individuals finished the two-year evaluations. After two years, no improvement in cognition was seen in the group as a whole. Specifically, those taking cocoa supplements showed no improvement in executive function, attention, episodic memory, or global cognition when compared to those receiving a placebo. Flavanols, a subclass of flavonoids that are naturally occurring in plants, fruits, and vegetables, are abundant in cocoa. Our trial results provide insight into the cognitive benefits of cocoa extract, said Dr. Chirag M. Vyas, the study’s first author.

The mechanism through which flavanols may improve cognition in individuals with poor diets is not explained by the study, but Dr. Vyas proposed the following theory: by lowering oxidative stress and inflammation, cocoa flavanols may improve cognitive function outcomes in older adults with poor diet quality. Studies have linked systemic levels of inflammation linked to cognitive aging and elevated oxidative stress in older adults with poor diets. Dr. According to Vyas’ theory, eating cocoa flavanols may lessen cognitive stressors and may also be influencing other neuroprotective processes. Over the course of a 12-week follow-up period, a 2021 trial found that cocoa flavonoids had a positive impact on cognitive aging. In addition to other plant compounds, nutritionist Kristin Kirkpatrick, who was not involved in the study, told MNT I advise clients to get plenty of flavonoids. and frequently suggest dark and cocoa chocolate as a fantastic choice with a wide range of culinary applications. Dr. According to Vyas, more investigation is required to clarify the weak link found in the study. Regarding the distinction between cocoa extract and actual cocoa or chocolate, Dr. Vyas replied, There is no simple answer to this question.. Due to compositional differences, the precise effects of chocolate, cocoa powder, and extract on cognitive health may differ, according to him. For instance, a particular compound is isolated to produce cocoa extract.

Even though the COSMOS cocoa extract supplement contains all of the naturally occurring bioactive components of the cocoa bean, we were unable to evaluate the effects of various formulations, separate cocoa extract components, or varying cocoa flavanol concentrations in this trial on cognitive benefits. According to Kirkpatrick, if someone is interested in the flavonoid benefits of cocoa beans, they should consume dark chocolate that is at least 75% cacao or use pure cocoa in their regular meals and snacks, such as topping applesauce or oatmeal with it. would supply that. Customers should search for that 100 percent cocoa, as pure raw cocoa usually contains no added sugar or fat, according to Kirkpatrick. You can use cocoa in a variety of ways, like adding it to yogurt or creating desserts like chocolate mousse. she continued. Dr. Vyas stated that he is not sure if he would advise consuming cocoa to improve cognitive function. According to the results of our trial, using supplements containing cocoa extract did not appear to improve cognitive function overall in older adults, he said. He is hesitant to guarantee a significant benefit just yet, even though the study indicates that older individuals who do not follow a healthy, balanced diet may benefit from consuming cocoa. Notwithstanding these encouraging results, more research is necessary to fully comprehend how cocoa flavanols affect cognition, particularly in more diverse populations and among those with lower-quality diets.

REFERENCES:

https://www.medicalnewstoday.com/articles/cocoa-extract-supplement-improves-cognition-older-adults
https://medicalxpress.com/news/2023-12-cocoa-supplement-benefits-cognition-older.html
https://www.sciencedaily.com/releases/2023/12/231207151255.htm
https://www.healthline.com/health-news/cocoa-extract-may-help-reduce-risk-of-cognitive-decline-in-older-adults

For medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com

Can protein predict mental decline before Alzhiemer’s sign?

Can protein predict mental decline before Alzhiemer’s sign?

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A protein called NPTX2 that is present in the cerebrospinal fluid may be able to forecast the onset of memory and cognitive issues, according to recent research.

Researchers evaluated people who had initially been in normal mental health but later experienced dementia or mild cognitive impairment (MCI).

According to the study, the quicker start of MCI symptoms was linked to lower levels of NPTX2. The results also demonstrated that NPTX2 levels, like other Alzheimer’s disease-related indicators, appear to fluctuate over time.

Findings from a recent study could be useful for understanding cognitive decline and early Alzheimer’s disease diagnosis.

The levels of a protein called NPTX2 in cerebrospinal fluid (CSF), or more simply put, the fluid surrounding the brain, were evaluated by the researchers in order to better understand the brain changes connected to moderate cognitive impairment and dementia.

Lower levels of NPTX2 were discovered to be associated with a more rapid beginning of cognitive deterioration. Along with other Alzheimer’s disease-related indicators, NPTX2 levels evolved with time.

Alzheimer’s disease indicators in cerebrospinal fluid measurement

The 269 participants in the BIOCARD Study who were initially in good mental health had their brain fluid (CSF) taken by the research team.

These patients were followed for an average of 16.3 years, and their average age at the start of the study was roughly 57.7 years.

Out of these people, 77 subsequently experienced dementia or Moderate cognitive impairment (MCI).

Quantitative parallel reaction monitoring mass spectrometry was used by the researchers to evaluate three similar peptides that make up the NPTX2 protein.

Three other markers—A42/A40, p-tau181, and t-tau—that are frequently linked to Alzheimer’s disease were also measured. These measurements were made using a Lumipulse automated electrochemiluminescence test on the identical CSF samples.

The goal of this data analysis was to help the researchers better understand how these indicators changed over time and whether they might be related to the onset of MCI and dementia in the patients under study.

NPTX2 levels and cognitive issues over time

They discovered that people with lower NPTX2 protein levels in their brain fluid (CSF) exhibited cognitive issues and memory deterioration (MCI) earlier than people with higher NPTX2 protein levels.

Both those who acquired MCI within seven years of the study’s beginning and those who did so later found this link to be substantial.

Even after accounting for other well-known Alzheimer’s disease markers detected in the CSF, the researchers observed that the baseline levels of NPTX2 were able to predict when the symptoms of MCI would manifest.

This implies that the amounts of these markers may be associated with modifications in NPTX2 and may contribute to the emergence of cognitive issues.

According to the study’s first author, Anja Soldan, Ph.D., an associate professor of neurology at Johns Hopkins University, “our study shows that low levels of the protein ‘neuropentraxin 2’ (or NPTX2) measured in the cerebrospinal fluid among cognitively healthy middle-aged and older adults may predict later onset of mild cognitive impairment (MCI).”

“[NPTX2] has been connected to learning and memory in mice in the past. Our findings add to the mounting evidence that low levels of this protein in individuals could signal MCI years before symptoms manifest. Notably, our results demonstrate that low levels of the protein enhance the prediction of cognitive impairment even when traditional Alzheimer’s disease biomarkers (such as those linked to amyloid plaques and tau tangles) and well-established genetic risk factors for late-onset Alzheimer’s disease are taken into account,” according to Dr. Anja Soldan.

According to Dr. Soldan, NPTX2 is “predictive of subsequent symptoms of MCI both within and beyond seven years before symptoms occurred.”

Limitations

The study does have a few drawbacks.

Namely that the majority of the participants were white, educated people with a history of dementia in their families. Therefore, it is uncertain whether the results apply to other populations, according to Dr. Soldan.

Without taking part in the study, Santosh Kesari, Ph.D., a neurologist at Providence Saint John’s Health Centre in Santa Monica, California, and the regional medical director for the Research Clinical Institute of Providence Southern California, told that “identifying blood or CSF biomarkers that predict developing dementia is critical to intervene earlier by preventative approaches or treat at the earliest onset of cognitive issues or even before when patients are aware they have dementia.”

Could this indicate new Alzheimer’s medications?

There is now just one FDA-approved treatment on the market that is known to even slightly reduce the signs of Alzheimer’s disease in its early stages, and there are no known therapies or strategies to avoid the disease, according to Dr. Soldan.

Our research demonstrates that reduced NPTX2 levels exist for many years before MCI or dementia brought on by Alzheimer’s disease, which increases the prospect of creating therapies that specifically target NPTX2.

Additionally, Dr. Soldan added, “Our findings may be relevant to other neurodegenerative diseases since this protein does not appear to be a specific marker for Alzheimer’s disease.”

Although significant work is being done to create sensitive methods of testing NPTX2 in blood rather than cerebrospinal fluid, we are not yet able to routinely measure brain levels of the substance in clinic settings. Another crucial area of research, according to Dr. Anja Soldan, is the factors that affect the levels of NPTX2 in the brain. However, we know very little about these factors.

Dr. Kesari concurred, stating that “NPTX2 may turn out to be a good target of drug development to prevent cognitive decline and will need to be further tested and validated in future studies.”

Future research will examine NPTX2 in more detail. In the end, additional study is required.

REFERENCES:

For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_239

Can a new Alzheimer’s vaccine cure or prevent the illness?

Can a new Alzheimer’s vaccine cure or prevent the illness?

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Finding a cure for Alzheimer’s disease has proven difficult and contentious. A vaccination has been created for a new target, a protein present in blood vessels and aging brain cells.

It has been tested on mice, and it enhances behavior while lowering levels of a protein precursor to amyloid-beta.

What molecules should be the focus of Alzheimer’s disease therapeutic research is still up for debate.

The development of amyloid beta protein plaques in the brain, which are defining symptoms of the disease, has been the focus of much of the research into treating Alzheimer’s disease. Using a mouse model, scientists have now created a novel vaccination that specifically targets a particular protein present in aging brain cells and blood vessels.

Recent years have seen debate concerning the history of the amyloid beta model and its application as a therapy target. For instance, there was debate about the efficacy and adverse effects of lecanemab (Leqembi) when the Food and Drug Administration (FDA) gave fast approval for its use in treating persons with early Alzheimer’s disease in January 2023. Particularly when the FDA did not, as anticipated, approve donanemab, an Alzheimer’s medicine made by the pharmaceutical corporation Eli Lilly because additional evidence was required to establish its efficacy.

When you think that finding a treatment target for Alzheimer’s disease is potentially big business for pharmaceutical companies, this explosive year for Alzheimer’s science may not have come as a surprise. There are presently 6 million cases in the United States alone, and it is predicted that number would increase to 13 million by the year 2050.

Importants facts about Alzhiemer’s disease

  • Alzheimer’s disease is a persistent, chronic (long-term) illness. It is not a normal ageing symptom.
  • Dementia and Alzheimer’s disease are not the same thing. A form of dementia is Alzheimer’s disease.
  • Its symptoms appear gradually, and its degenerative effects on the brain result in a steady decline.
  • Alzheimer’s disease can affect anyone, but some people are more susceptible to it than others. People over 65 and those with a family history of the illness are included in this.
  • Alzheimer’s patients cannot be predicted to have a particular outcome. While some persons experience a slower onset of symptoms and a faster rate of disease progression, others experience lengthy lifespans with minor cognitive impairment.

A vaccination for Alzheimer’s disease may also target atherosclerosis.

Inflammation is one of the other pathways known to contribute to the development of Alzheimer’s disease. There is some disagreement as to whether or not atherosclerosis and inflammation are related diseases. Inflammation also underlies other disorders.

Vasculature and inflammation are involved in both disorders. People with specific APOE gene variations are known to be predisposed to both disorders.

For around ten years, mouse models have been used in the research and development of potential treatments for both disorders.

Researchers in Tokyo found that senescence-associated glycoprotein (SAGP-protein) was elevated in immunological and vascular endothelial cells in animal models with atherosclerosis as one recent example of this. In animal models with mutations on the APOE gene, greater expression of this protein has been connected to an increased risk of atherosclerosis and Alzheimer’s disease. Around the immune cells called microglia in the brain, SAGP-protein is also present.

The team’s prior research has demonstrated that decreasing the expression of this protein reduces atherosclerotic plaques in the aorta of mice with APOE gene variations and improves glucose metabolism in obese animals.

They also disclosed that they had created a vaccination that specifically targeted older cells with high levels of SAGP-protein expression.

The same research recently revealed they had found this vaccine may also lessen levels of inflammatory chemicals and amyloid-beta peptide, which is a precursor to amyloid beta protein and affects how Alzheimer’s disease behaves in mice models.

These preliminary research findings were presented at the Basic Cardiovascular Sciences Scientific Sessions of the American Heart Association in Boston in 2023.

A new Alzheimer’s vaccine may change the game.

In an email, the study’s lead author, Dr. Chieh-Lun Hsiao, stated: “Unfortunately, how we generate vaccine is not allowed to expose, but the design of the vaccine is to eliminate or reduce the cells which contain an abundance of our target, SAGP.”

How the vaccination functions are described by Dr Hsiao as follows:

The immune system is trained through vaccination to recognize a particular foreign substance, such as an antigen or peptide. In our theory, we would say that we hypothesize that the pathogenic/abnormal cells with elevated SAGP expression.

Therefore, following vaccination, individuals would have the immunity necessary to recognize SAGP-HIGH expressed signal and then remove/destroy the cells that contain SAGP-HIGH expressed signal.

The study’s authors concluded that Alzheimer’s disease might someday be treated with their vaccine.

In the future, we’d probably switch to different animal models for more in-depth research on vaccination effectiveness, according to researcher Dr Hsiao. We are also interested in how different cell types’ phenotypes alter in response to immunisation. As we move forward, we’ll pay greater attention to the mechanisms.

Potential drawbacks and effects of the new vaccine

There needs to be more research on the potential negative consequences of this target, according to Kath Intson, CEO of the Canadian business Variant that specialises in precision medicine and a PhD candidate at the University of Toronto.

In an email, Intson stated:

“At best, there is a low likelihood that a medication like this will be used prophylactically, or like a vaccination, to prevent AD. One of the targets is microglia, which function similarly to immune cells in the brain. I’m interested in learning more about the percentage of SAGP-enriched, highly enriched microglia that were removed. As you might expect, eliminating a significant portion of the brain’s immune system has negative effects.”

She also questioned whether Alzheimer’s disease treatments should focus on preventing the accumulation of amyloid-beta peptide (APP), the precursor of amyloid beta-protein: “One point – we must cease thinking of APP accumulation as a fundamentally abnormal physiological process.”

Previous research has shown that APP acts as a protective factor in the brain after acute lesions like strokes or traumatic brain injuries. In response to these assaults, APP overexpression increases brain cell survival in the near term. Any suggestion of mass vaccination campaigns with APP-elimination goals has my utmost scepticism. It would have effects on the health of healthy people about other brain-damaging disorders to remove this necessary and typical function.

REFERENCES:

For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_239

Does Alzhiemer’s symptoms worsen due to light sensitivity?

Does Alzhiemer’s symptoms worsen due to light sensitivity?

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The late afternoon and evening are when sundowning, a characteristic of Alzheimer’s disease, typically manifests. Increased agitation, anxiety, and mood fluctuations are some of its defining characteristics.

The impact of Alzheimer’s disease on the brain has been suggested as one of the causes, however the exact mechanisms remain unclear.

Increased light sensitivity was shown in recent studies using Alzheimer’s disease mice models, which is a result of retinal alterations.

Sundowning is a crippling symptom of Alzheimer’s disease that makes people’s dementia symptoms get worse in the late afternoon and evening.

Some researchers hypothesised that this symptom was caused by brain abnormalities, and a recent study confirmed that immune cells in the brains of Alzheimer’s patients may experience circadian disruptions that increase the accumulation of amyloid beta.

One of the distinguishing features of Alzheimer’s disease is the accumulation of this protein. A psychiatrist from the Rehab Clinics Group named Dr. Alexander Lapa stated in an email:

Both the affected person and their carers may find sunseting upsetting. Increased care requirements and potential major disruptions to daily routines can result from the increase in bewilderment and agitation. Sundowning in some circumstances could endanger the patient’s safety or the safety of those around them.

He continued by saying that many doctors advise individuals with Alzheimer’s disease to follow a daily regimen that includes predictable timings, relaxing hobbies, reducing noise, and making sure there is enough illumination at night.

Increased light sensitivity in Alzheimer’s mice models

The aetiology of sundowning is unknown, despite the incapacitating nature of this symptom of Alzheimer’s disease. Given that it manifests in the middle and late phases of the disease, it may coexist with a number of other symptoms that have all been connected to sundowning, including sleep disturbances, forgetting to eat or drink, and adverse drug reactions.

A group of researchers from the University of Virginia, Charlottesville, Virginia, chose to further explore this connection because sleep disturbance has previously been closely linked to Alzheimer’s disease. Their research was published most recently in Frontiers to Ageing Neuroscience.

It had been thought that sleep disturbance might also result from damage to the brain brought on by the buildup of tau protein and amyloid beta protein, two signs of Alzheimer’s disease.

According to the main author Dr. Heather Ferris, an assistant professor of medicine at the University of Virginia, “We were interested in why sleep and circadian rhythms are disrupted in Alzheimer’s disease.”

After ruling out a number of potential causes in the brain, she stated, “We turned our attention to the retina because we thought the problem would be occurring in the brain.”

According to Dr. Ferris, the retina contains specialized cells known as inherently photosensitive retinal ganglion cells. Although these cells are sensitive to light, they are not used for vision. Instead, these cells are employed to inform the brain that it is daytime.

We discovered that we could activate these cells in Alzheimer’s disease model mice with much less light and that the retina contained a greater number of these cells, she said.

Looking for the cause of the sundowning

Researchers first employed mice models with genetic alterations that resembled Alzheimer’s disease, along with controls, to learn this. To simulate jet lag, they first gave 13-month-old female mice a 6-hour change in their exposure to sunshine before going back to a regular 24-hour schedule.

They discovered that Alzheimer’s disease-affected mouse models retrained to a 24-hour clock pattern more quickly than control mice.

The initial theory put forth by researchers was that this difference resulted from a higher concentration of microglia, a kind of immune cell present in the brain that surrounds amyloid beta plaques and works to eliminate them.

However, fewer microglia in the Alzheimer’s disease mouse models did not result in a quicker recovery to a typical 24-hour cycle after jet lag.

Researchers then found that mouse models of Alzheimer’s disease were more likely than wild-type mice to behave differently in response to changes in lighting, indicating that they were more sensitive to light reception.

The researchers came to the conclusion that Alzheimer’s disease affects the retina rather than the brain as a result of this discovery.

The retina contains the photosensitive cells that control circadian rhythms. The light-sensitive protein that they produce, called melanopsin, is located in the retina and is what we saw in Alzheimer’s disease mice, according to Dr. Ferris, even though they travel through the optic nerve to interact with the brain.

How to possibly handle sundowning?

This hypothesis is supported by prior research, which has shown that amyloid and tau proteins can be found in the retina of people with Alzheimer’s disease and that this condition also causes the retinal blood barrier to break down.

The discovery that the retina in a mouse model of Alzheimer’s disease may be impacted in a way that increases light sensitivity may point to novel strategies for coping with dusk.

In the future, Dr. Ferris stated she hoped to test this notion. To maintain rhythms as close to normal as possible, she added, doctors currently advise keeping persons with Alzheimer’s disease on a rigorous schedule for eating, sleeping, and light exposure.

She suggested that light treatment might provide the solution.

According to our findings, these efforts might be thwarted by lower levels of light than might be anticipated. To increase the effectiveness of these therapies, we plan to examine next whether we can reduce exposure to light at particular periods or alter its wavelength to prevent some behavioral changes.

Beyond maintaining a regular schedule, she continued, “It makes sense to try to reduce evening exposure to blue light (screens) as this type of light is most likely to trigger melanopsin and disrupt sleep and circadian rhythms — whether you have Alzheimer’s disease or not.”

REFERENCES:

For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_239

MIND diet: Can it assist in improving cognitive ability?

MIND diet: Can it assist in improving cognitive ability?

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People may start to notice a minor slowdown in processing speed and sporadic memory lapses as a result of ageing or an age-related illness like dementia.

Although these results have not been replicated in clinical trials, diet may provide protective advantages against cognitive deterioration.

An older person’s cognition may be improved by reducing daily caloric consumption by a small amount, according to a recent study.

Improvements in cognition were similar for those on the MIND diet and those on any minor calorie restriction, with no significant differences between the two groups.

As we age, cognitive change is typical. Even in your 20s and 30s, you may notice a modest reduction in memory and processing speed, however this is typically accompanied by advances in accumulated knowledge well into old age.

Observational studies imply that the Mediterranean diet may have positive effects on cognition, despite the fact that no specific vitamin has been found to stop cognitive decline.

The MIND diet, a combination of the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets, and mild calorie restriction have now been examined for their impact on cognition.

Both diets had a somewhat positive impact on cognition, according to the study, but neither was noticeably superior to the other.

“This study results point to mild caloric restriction and an average weight loss of 5.5% as lifestyle factors that may support cognition in older adults,” said Molly Rapozo, a registered dietitian nutritionist and senior nutrition and health educator at the Pacific Neuroscience Institute in Santa Monica, California.

The MIND diet: what is it?

The acronym “MIND” refers to “Mediterranean-DASH Intervention for Neurodegenerative Delay.”

The MIND diet seeks to lessen dementia and the deterioration of brain health that frequently happens as people age. It combines elements of the Mediterranean diet with the Dietary Approaches to Stop Hypertension (DASH) diet, two highly well-known eating plans.

The DASH diet and the Mediterranean diet are two of the healthiest diets, according to many experts. They can lower blood pressure and lower the risk of heart disease, diabetes, and a number of other ailments, according to research.

However, scientists sought to develop a diet designed particularly to support better brain health and guard against dementia.

They mixed foods from the DASH and Mediterranean diets, which have been demonstrated to improve brain function, to achieve this.

For illustration, both the DASH diet and the Mediterranean diet advise consuming lots of fruit. Berries in particular have the greatest supporting data, although eating fruit in general has been related to increased brain function.

So, while the MIND diet does not emphasize fruit consumption in general, it does advocate eating berries.

As of right now, there are no fixed rules for adopting the MIND diet. You can easily increase your consumption of the 10 items that the diet suggests and decrease your consumption of the 5 foods that it advises you to limit.

Cutting calories may benefit the brain.

A total of 604 participants were enlisted in the study by the researchers. Despite eating poorly and reporting a family history of Alzheimer’s, none of the participants tested negatively for cognitive deterioration. Body mass index (BMI) > 25 (overweight) was present in each individual.

The participants were randomized into two groups at random: 301 individuals were assigned to the MIND diet, and the remaining 303 individuals continued to follow their regular dietary regimen.

Additionally, as one of the study’s objectives was to reduce body mass by 3-5%, the researchers decreased everyone’s daily calorie consumption by 250 calories.

For three years, the participants were instructed to stick to their diet, and throughout that period, they received frequent dietary counselling over the phone and in person. To make sure both groups were getting the right amount of calories, advice was given about portion size. The MIND diet participants also received instructions on which new meals to incorporate and which ones they should avoid.

Four times over the three years, the researchers checked in with the individuals to evaluate their mental functioning, blood pressure, diet, level of physical activity, and usage of medications.

Participants had a variety of cognitive tests administered by researchers who were not aware of which diet group they were in after six months, then at 12, 24, and 36 months. To detect any abnormalities in the brain, some also had magnetic resonance imaging (MRI) scans.

Inflammation and oxidative stress are reduced by the MIND diet?

The particular mechanisms by which the MIND diet operates are yet unknown, according to the available research. However, researchers believe that it might function by decreasing inflammation and oxidative stress.

Free radicals, which are unstable chemicals, build up significantly in the body and cause oxidative stress. Cells are typically harmed by this. Particularly susceptible to this kind of harm is the brain.

Your body naturally responds to injury and infection with inflammation. However, inflammation can also be damaging and a factor in many chronic diseases if it is not well controlled.

Inflammation and oxidative stress can both hurt your brain. They have been the focus of some recent Alzheimer’s disease prevention and treatment initiatives.

Lower levels of oxidative stress and inflammation have been linked to following the DASH and Mediterranean diets.

The MIND diet is a combination of these two diets, thus the foods that make up the MIND diet likely also have antioxidant and anti-inflammatory benefits.

By shielding the brain from oxidative stress, antioxidants in berries and vitamin E in olive oil, green leafy vegetables, and almonds are thought to improve brain function.

Omega-3 fatty acids, which are present in fatty fish, are also well known for their capacity to reduce brain inflammation and have been linked to a slower loss of cognitive function.

The dangerous beta-amyloid proteins may be reduced by the MIND diet.

Researchers think that by lowering potentially hazardous beta-amyloid proteins, the MIND diet may also benefit the brain.

Protein fragments called beta-amyloid proteins can be found in the body naturally. However, they can assemble into plaques that develop in the brain, obstructing neural connections and ultimately resulting in the death of brain cells.

In fact, a lot of scientists think that these plaques are one of the main reasons why Alzheimer’s occurs.

Studies on animals and in cells indicate that the antioxidants found in several MIND diet items may aid in preventing the development of beta-amyloid plaques in the brain.

The Summary

The MIND diet was developed to decrease the deterioration of brain function that can occur with ageing and prevent dementia. The diet promotes the consumption of fruits, vegetables, whole grains, olive oil, fish, chicken, beans, and wine.

These meals provide a variety of nutrients that support healthy brain function, perhaps by lowering oxidative stress, inflammation, and beta-amyloid plaque development.

According to preliminary study, strictly adhering to the MIND diet is linked to a lower risk of Alzheimer’s disease and a slower decline in brain function over time. To fully comprehend the consequences of the diet, more research is required.

Future study revealing that the MIND diet provides additional health advantages linked to the Mediterranean and DASH diets won’t come as a surprise because it is a combo of these two diets.

But for now, the MIND diet is a terrific and easy-to-follow method if you’re seeking for a way of eating that focuses on maintaining brain function as you age.

REFERENCES:

For Mental disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?therapy=83

Cognitive function: Can better sleep absorption improve it?

Cognitive function: Can better sleep absorption improve it?

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The association between obstructive sleep apnea, insufficient sleep, and cognitive performance was further explored in a new research that examined data from five population-based studies.

Greater sleep consolidation and preventing obstructive sleep apnea, in which breathing is interrupted while sleeping, were connected to greater cognitive function in the subjects, according to the data.

On the other hand, less sleep was associated with concerns like poor focus and other cognitive problems.

According to a study published in JAMA Network Open, sleep consolidation and the absence of obstructive sleep apnea may be crucial for enhancing cognition with ageing in persons without dementia.

Data from five population-based studies conducted across the United States with at least five years of follow-up were examined by researchers. Studies included cognitive tests and nightly sleep studies. They examined the information from March 2020 to June 2023.

The researchers examined sleep studies that focused on sleep apnea and sleep consolidation and their relationships to dementia risk as well as associated cognitive and brain function.

5,945 persons without a history of stroke or dementia participated in the study.

The results showed that longer sleep duration was linked to better attention and processing speed, while better sleep consolidation and the absence of obstructive sleep apnea were related with worse cognitive function.

Sleep that is uninterrupted by nighttime awakenings and is continuous is referred to as consolidated sleep. The hallmark of obstructive sleep apnea is episodes of airway collapse, which can lower oxygen levels and lead to fragmented, unrestorative sleep.

What can we learn from this sleep study?

Over the course of the 5-year follow-up, the researchers discovered that stronger sleep consolidation and the lack of sleep apnea were related to better cognition.

The researchers hypothesised that these results demonstrated the necessity for additional study on the effect of therapies in enhancing consolidated sleep to preserve cognitive function.

“Some aspects [of this study] were predictable and further reinforced concepts related to the association between sleep and cognition over time,” said Dr. Vernon Williams, a sports neurologist, pain management expert, and founding director of the Centre for Sports Neurology and Pain Medicine at Cedars-Sinai Kerlan-Jobe Institute in Los Angeles who was not involved in the research.

The lack of a correlation between cognitive deterioration and particular sleep stages was an intriguing and less expected finding in this study. A decrease in slow-wave, deep sleep would have been expected to be more harmful than other stages, however this was not the case. Though there are a lot of plausible answers, that is a fascinating discovery, said Dr. Vernon Williams.

Dr. Williams continued, “This study [further] helps by demonstrating effects across multiple participant groups and by demonstrating that overall sleep efficiency, as well as the presence of obstructive sleep apnea, significantly affect cognition over time, whether or not a prior diagnosis exists.”

Obstructive sleep apnea: What is it?

Breathing pauses during sleep are a common symptom of obstructive sleep apnea. According to the National Heart, Lung, and Blood Institute, it restarts frequently while you sleep.

According to medical professionals, between 9 and 17% of women and between 25 and 30% of males are believed to suffer from obstructive sleep apnea. Age increases prevalence.

The most prevalent kind of sleep apnea is caused by a collapse or restriction of the upper airway, which prevents airflow. When this occurs, the person briefly stops breathing before restarting it while they are sleeping, and they normally are not aware of it.

It may result in restless sleep, difficulty focusing, and issues with memory and decision-making.

The American Lung Association lists the following as symptoms of sleep apnea:

  • snoring
  • daytime slumber
  • breathing breaks
  • memory and attention issues
  • Moodiness and annoyance
  • frequent nighttime awakenings for urination
  • daily headaches
  • mouth arid.

It is connected to other medical issues as well. Obstructive sleep apnea may increase the risk of high blood pressure, diabetes, heart disease, and stroke, according to research.

How to lessen the symptoms of sleep apnea

A functional medicine physician and health and wellness coach named Dr. Laura DeCesaris, who was not involved in the study, stated that lifestyle modifications like decreasing weight, quitting smoking, and abstaining from alcohol can lessen obstructive sleep apnea.

She also provided the following advice for enhancing sleep:

  • Managing stress more skillfully and paying attention to where the body stores stress can help prevent forward head carriage and other breathing problems. Many people hold tension in their necks and shoulders.
  • monitoring your sleeping position, as side sleeping can occasionally aid with symptoms
  • Since chronic inflammation in the gut and nasal passages frequently makes it difficult to breathe through the nose, changing the diet and, when possible, switching to a more anti-inflammatory diet may be helpful.
  • exercising consistently
  • Especially in a dry area, remember to stay hydrated and consider installing a humidifier in your bedroom.

REFERENCES:

For Mental disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

Cognitive decline: What causes and slow it down.

Cognitive decline: What causes and slow it down.

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Age-related cognitive and memory deterioration is a universal phenomenon, however the specific causes are yet unknown to science. While some lifestyle choices can prevent cognitive decline, age-related illnesses like dementia speed it up.

One recent study using mice models may now have identified the primary mechanism underlying the cognitive impairment brought on by typical aging.

Another recent study, this one using mice, raised the possibility that social connection, cognitive training, and physical activity could halt the ageing process and prevent cognitive deterioration.

As we become older, our cognitive abilities—the brain processes that enable thinking, learning, memory, awareness of one’s environment, and judgment—change. Our capacity to process information and make decisions swiftly decreases as our brain’s nerve cells and synapses age.

Most people begin to notice a steady deterioration at around age 50. However, advances in cumulative knowledge continue far into old life together with this minor decline in processing speed and working memory.

But why are the changes happening? According to a recent study conducted on mice, changes in a brain protein may limit synaptic plasticity, the capacity of nerve cells to change the strength of their connections, which impairs memory. This research is published in Science Signalling.

We may be able to prevent age-related cognitive loss, according to a different study conducted on mice. In this study, which was published in the journal Ageing, researchers hypothesise that social interaction, mental exercise, and physical activity all work to activate an enzyme that enhances the functionality of nerve cells and synapses, enhancing cognitive performance.

What leads to cognitive ageing?

The first study focused on CaM kinase II (CaMKII), an enzyme that is involved in synaptic plasticity and the transmission of nerve impulses across synapses, among other functions.

They simulated the cognitive effects of typical ageing in mice by changing this brain protein.

Nitric oxide (NO), according to earlier research by the same authors, may influence CaMKII’s function. This work expanded on previous investigation and discovered that CaMKII is modified via a procedure termed S-nitrosylation, which depends on NO.

Memory and learning skills are hampered if CaMKII’s nitrosylation is diminished, which occurs with natural ageing.

Prof. Ulli Bayer, of the University of Colorado Anschutz School of Medicine and the study author, outlined the potential causes of this.

He explained to us that the diminished nitrosylation of CaMKII results in a decrease in its synaptic localisation, which appears to impede its synaptic activities.

Simply put, a decrease in NO decreases the transmission of nerve impulses through the synapses between nerve cells, which may contribute to cognitive deterioration.

Cognitive decline and way of life

The benefits of a healthy lifestyle on brain health have long been recognised by researchers. According to a 2015 study, exercise, intermittent fasting, and critical thinking are crucial for maintaining good brain function over the course of a person’s lifetime.

In people with normal cognition, a healthy lifestyle is linked to a slower rate of memory impairment, according to another extensive study.

Social connection, physical activity, and cognitive training are all positive experiences that are beneficial to cognitive health. The precise mechanism by which these lifestyle factors work is unknown.

A mechanism that could explain how these satisfying events improve your brain health has now been discovered by the Ageing study, which was carried out in mice.

For ten weeks, the researchers kept adult and senior mice in an enhanced environment. They were housed in huge cages with bedding, a cardboard tube, a running wheel, many plastic toys (tunnels, platforms, see-saws), and a metal ladder in groups of eight to ten mice each. Twice per week, the toys were rearranged, and once per week, new toys were added.

The only items in the control group’s regular cages, which were housed in groups of two to four mice each, were bedding and a cardboard tube.

The researchers tested the cognitive abilities of both groups once every week using land and water mazes. These were put to the test:

  • working memory for space the capacity to temporarily maintain spatial information engaged in working memory.
  • cognitive adaptability, or the capacity to change with the environment
  • Long-term recall of task-related spatial, factual, and contextual elements is known as spatial reference memory.

How enrichment keeps cognitive ability intact?

Comparing mice in the usual environment to those in the enriched environment, the mice in the enhanced environment performed better on every behavioural task. The elder mice showed a particularly noticeable improvement.

“Our study provides a potential mechanistic basis for the effects of enrichment — this removes the ‘wooliness’ associated with such enrichment studies and puts them on a more rigorous scientific basis,” said Prof. Bruno Frenguelli, corresponding author and a professor of neuroscience at the University of Warwick in the United Kingdom.

In mice with a mutation in the enzyme MSK1, which is involved in neural growth and synaptic plasticity, the researchers did not observe any advantages.

They came to the conclusion that MSK1 is necessary for enrichment to fully improve cognition, synaptic plasticity, and gene expression.

The following is how Prof. Frenguelli explained it to us:

MSK1 is an enzyme that controls gene expression, or more specifically, it stimulates the activation of a variety of genes. We believe that MSK1 influences cognition by turning on a number of these genes because they have been linked to various aspects of learning and memory.

Exercise, networking, and ongoing learning

“Although our mechanistic experiments were conducted in mice, earlier research has revealed that ageing reduces CaMKII’s nitrosylation in both mice and humans. Pharmacological therapies should be able to boost CaMKII’s nitrosylation and so reduce the cognitive losses related to normal ageing, according to Dr. Bayer.

While there are currently no such treatments, research is being done, as Dr. Bayer stated: “This needs further research/development, but there are actually candidate approaches — such as inhibitors of GSNOR, an enzyme that limits nitric oxide bioavailability, and that is higher expressed with aging.”

The second study, however, suggests that we might not have to wait for pharmacological treatments to stop cognitive ageing. Prof. Frenguelli provided an explanation of why lifestyle enrichment should be effective in both humans and mice.

“A key brain growth factor (BDNF), which activates MSK1, has been implicated in both rodents and humans as being important for these benefits,” he said.

“By identifying key molecules involved in this process, this offers opportunities to explore and exploit these molecules as drug targets,” the author continued.

And he added that you can never be too old to reap the benefits of physical activity, interpersonal contact, and mental stimulation: “Our recent findings show that these benefits occur even in very old mice (equivalent to 70s in humans), meaning that it’s never too late to offer and engage in such enrichment activities to elderly people.”

How do medical professionals spot cognitive decline?

If you’re unsure if you’re exhibiting usual ageing symptoms or cognitive decline indications, a doctor can help. For a quick self-screening exam to look for signs of cognitive deterioration, they might provide you.

Other screening exams, such as the Self-Administered Gerocognitive Examination (SAGE),

You can use a variety of screen tests to look for indicators of cognitive impairment. These exams typically last between three and fifteen minutes. They consist of:

  • Self-Administered Gerocognitive Examination (SAGE)
  • AD8 Dementia Screening Interview
  • Quick Dementia Rating System (QDRS)
  • Mini-Cog

One of the most popular screening exams is SAGE. The test is available for download online, and you can take it offline. You might even finish it off at a doctor’s office.

SAGE is unique from the other tests because it is a little bit more complicated. According to a 2022 study, SAGE identified cognitive impairment in MCI patients six months earlier than the MMSE, another popular test. A review from 2021 found that SAGE delivers the right answer 79% of the time.

Please take note that these brief tests alone cannot identify cognitive impairment or dementia. A doctor may need to conduct a more complete evaluation if your score starts to fall.

REFERENCES:

For Mental disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

Alzheimer’s disease: Loss of smell may be the sign?

Alzheimer’s disease: Loss of smell may be the sign?

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More than 6 million people in the United States are affected by Alzheimer’s disease, which is the most prevalent type of dementia.

The key to controlling the condition is early detection, yet first symptoms like memory problems are frequently written off as normal aging symptoms.

According to a recent study, those who contain the APOE4 gene mutation, who are more likely to acquire Alzheimer’s disease, may begin to lose their sense of smell sooner than people who do not.

Testing people’s sense of smell could assist identify those at higher risk of Alzheimer’s because this reduced sense of smell may be an early marker of future cognitive issues.

Around 1 in 9 Americans over the age of 65, or 6.7 million people, have Alzheimer’s disease (AD), according to the Alzheimer’s Association. By 2050, scientists predict that this number will surpass 12 million due to an ageing population.

Alzheimer’s is a degenerative, incurable disease, but it is not a natural part of becoming older. If a person begins to have memory issues or cognitive deficiencies, these should not be ignored as normal ageing symptoms because early diagnosis enables effective therapy.

Globally, 13.7% of the population carries the APOE4 gene variation, which raises the risk of Alzheimer’s disease. 40% of those who are diagnosed with the illness have this gene.

According to a recent study in Neurology, those who have this gene mutation may have a compromised sense of smell before they show any signs of Alzheimer’s disease, like moderate cognitive impairment.

The researchers propose that screening for odour sensitivity may be helpful for identifying those who are at risk.

Alterations in scent brought on by Alzheimer’s

In order to conduct the study, 865 participants responded to a survey that measured their capacity for odour detection as well as their ability to identify the odour. Every five years, they underwent testing.

Additionally, they conducted two tests of their memory and thinking, with a five-year gap between each test.

Who carried the gene mutation that enhanced risk for Alzheimer’s disease was determined by DNA testing. Based on the concentration of an odour that participants had to be exposed to in order to notice it, scores ranged from zero to six.

The study’s team discovered that those with the APOE e4 allele had a 37% lower likelihood of being adept at smelling things than those without it. This came after age, sex, and education were all taken into account.

Between the ages of 65 and 69, odour detection started to decline.

It wasn’t until participants reached the ages of 75 to 79 that changes in their capacity to detect the smell started to show. However, compared to people without the Alzheimer’s gene variation, once they lost the capacity to name smells, this skill deteriorated more quickly.

Those who had the gene mutation also aged more quickly in terms of cognitive decline.

Losing one’s sense of smell could be an early sign of Alzheimer’s.

Over the course of the trial, those who had the gene were 37% less likely than those who did not to have effective odour detection.

Age-related loss in odour sensitivity was observed in those with the APOE 4 variant at 65 years of age, as compared to those without the gene. However, non-carriers, who initially had a greater sense of smell, showed a faster drop beyond the age of 65.

At 65, there was no difference between carriers and non-carriers in their capacity to recognise odours, but this ability started to diminish more quickly in carriers, especially around age 75. Similar trends were seen in cognition, with those with the APOE 4 variation seeing quicker decreases in cognition.

Although the researchers did not discover a connection between odour detection and cognition, their data do imply a connection between odour identification and cognition.

The authors discovered that APOE 4 carriers had odour sensitivity impairments that manifested sooner in life (65–69 years old) than odour identification impairments (75–79 years old), according to Dr. Clark, who was not involved in the study. Additionally, among APOE 4 carriers, odour sensitivity deficiencies came before cognitive deterioration.

She continued, “This shows that reduced odour sensitivity may be an early indication of future cognitive impairment in APOE 4 carriers.”

How to lower your chance of getting Alzheimer’s?

In addition to not participating in the study, Dr. Alejandro Alva is the founder, chief medical officer, and CEO of Pacific Neuropsychiatric Specialists (PNS). He also stated that there are other risk factors besides age that can contribute to an increased number of people developing Alzheimer’s disease.

Sedentary behavior, obesity, smoking, excessive drinking, high blood pressure, and other things are among these risk factors.

However, according to Alva, there are several lifestyle modifications that can lower your risk and enhance your general health. He offers the following advice:

  • Control your blood pressure. Alva suggests following any medical advice, eating a range of heart-healthy foods, and keeping your salt intake under 5 g per day.
  • Continue your usual exercise regimen. 150 minutes per week of aerobic exercise helps reduce risk, especially when combined with other aspects of a healthy lifestyle.
  • Stop drinking excessively. “Drinking alcohol can increase the loss of brain cells and can induce the accumulation of toxic protein in the brain,” he said. “It is advised to drink in moderation or to completely kick the habit.”
  • Give up smoking. “The chemicals and toxins from cigarettes can cause inflammation and stress on brain cells that can significantly increase the risk of Alzheimer’s disease,” claimed Alva.

The development of Alzheimer’s disease can be delayed or slowed down with the use of certain drugs, Alexander continued.

Lecanemab (Leqembi) and aducanumab (Aduhelm) are two FDA-approved drugs that are being used to control the illness, according to the Alzheimer’s Association.

She added, “However, individuals may be able to lower their chances of acquiring this degenerative condition by adopting preventative actions and identifying one’s risk factors.

Summary

An association between the loss of scent and the later onset of Alzheimer’s has been discovered by recent research. People with a certain gene variant known as APOE e4 were the ones that showed this connection.

According to experts, the loss of smell may be utilized to anticipate future cognitive issues. Your risk of Alzheimer’s may be lowered by making certain lifestyle decisions. Additionally, several drugs might stop it in its tracks.

REFERENCES:

For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_239