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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

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

Resist age-related cognitive decline with daily probiotics.

Resist age-related cognitive decline with daily probiotics.

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According to the outcomes of a scientific experiment, those with mild cognitive impairment who took a probiotic for 30 days performed better on cognitive tests.

After the trial, those who took probiotics had lower levels of a type of bacteria linked to cognitive impairment in their gut microbiomes.

According to the research, altering gut flora may be a promising strategy for treating chronic illnesses like cognitive impairment.

Probiotic therapy may help persons with moderate cognitive impairment (MCI) regain cognitive function, according to a clinical investigation.

There is an urgent need for more research,” declared Mashael R. Aljumaah, the primary study author and a doctorate candidate in microbiology at the University of North Carolina at Chapel Hill, in light of the global rise in dementia and Alzheimer’s disease (AD).

People with cognitive impairment were given daily probiotics of Lactobacillus rhamnosus GG during the double-blind randomised study. Also, after three months, their cognitive test results improved.

The researchers examined the participants’ stool samples and discovered significant quantities of Lactobacillus rhamnosus GG, or LGG, as well as a decrease in the quantity of Prevotella, a different family of bacteria frequently detected in individuals with cognitive deterioration.

These alterations imply a favourable change in the microbiota makeup of the subjects.

“Numerous earlier animal investigations, which showed LGG’s beneficial effects on several physiological situations, led to its development as a possible therapeutic probiotic. As a probiotic, LGG is also well-known for its capacity to withstand acidity and stick to intestinal walls,” according to lead researcher Michael R. Aljumaah.

Probiotic’s effects on mild cognitive impairment

To conduct the study, researchers contrasted those who had minor cognitive impairment with those who did not.

They aimed to spot, comprehend, and try to sway the early phases of cognitive deterioration. Finding biomarkers that could indicate the onset of cognitive decline was a part of that endeavor.

The age range of the 169 participants in the clinical trial ranged from 52 to 75 years old. As a control group, those without cognitive disorders were assigned to one group. People with cognitive problems were assigned to another group.

For three months, either LGG or a placebo was given to both groups. There were no negative effects in either group.

Prevotella, one such biomarker, was discovered in adults with cognitive impairment by Aljumaah and her coworkers. The fact that receiving LGG seemed to lessen its presence points to a potential future for microbiome re-balancing.

Aljumaah added, “By developing microbiome-targeted therapies, we may be able to delay the onset of cognitive impairment.”

Prevotella bacteria and long-term illnesses

Aljumaah clarified that while the Prevotella family of bacteria is present in persons with cognitive loss, it is not totally evident that their effect is solely detrimental.

For instance, the bacteria Prevotella has been linked to autoimmune, inflammatory, and cognitive disorders. According to Aljumaah, it is frequently discovered in persons who have Crohn’s disease or inflammatory bowel disorders such rheumatoid arthritis (RA).

Additionally, because it originates from plant-based diets, Prevotella bacteria may aid in the processing of fiber and is linked to metabolites that are crucial for maintaining gut health.

This raises the question of whether specific Prevotella species or strains may contribute to these illnesses, or whether a particular genetic characteristic or mechanism may be to blame, Aljumaah observed.

Greater research with LGG bacteria is required.

Board-certified neurologist Dr. Santosh Kesari, director of neuro-oncology at the Pacific Neuroscience Institute in Santa Monica, California, who was not involved in the study, told MNT that he considered the participants’ receiving cognitive advantages “intriguing.”

However, Dr. Kesari urged further investigations to confirm their findings and make sure that adding LGG bacteria doesn’t have any negative side effects.

He also raised concern that an attempt to treat a condition by adding a probiotic to the gut microbiome would upset the bacterial equilibrium, leading to negative effects.

“Focusing on a positive effect on brain health could have a counterproductive effect in another organ system,” Dr. Kesari warned.

Health effects of the gut-brain relationship

It’s crucial to keep in mind that our knowledge of the precise pathways tying the gut microbiome to cognitive function is still in its infancy, according to Aljumaah.

According to Aljumaah, “more specifically, our understanding about which members of the gut [microbiome] are involved remains limited.”

Aljumaah also suggested a number of potential routes for communication between the two dispersed bodily regions, including the vagus nerve and the immune system.

Additionally, metabolites like short-chain fatty acids and even neurotransmitters made by the gut flora may be implicated.

Dr. Kesari proposed that the microbiome’s influence on brain function might be more indirect.

The microbiome is really the doorway for nutrition, nutrients, and how things are metabolized, according to Dr. Kesari, therefore it has a huge impact on overall body health, including brain function. “You are what you eat, as the saying goes, and this is really the scientific proof of that,” said Dr. Kesari.

Improving health outcomes by changing the microbiome

Undoubtedly, the microbiome is medicine’s most challenging and exciting frontier in terms of human health. Prevotella serves as an illustration of how the microbiome is likewise a challenging field of research.

Whether or not researchers can ever fully comprehend the microbiome to control or rebalance its residents, Dr. Kesari said, “I think it has to get there.”

We are aware that nutrition and obesity are the main causes of morbidities in the United States. Many of these conditions are preventable, and the microbiome plays a role in some of them. There is no chance that our eating patterns will change very soon. So, in my opinion, the only solution to lessen the cost pressures of healthcare is if we can obtain a probiotic that may help us stay healthier, said neurologist Dr. Santosh Kesari.

REFERENCES;

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

Can Obstructive sleep apnea cause cognitive decline?

Can Obstructive sleep apnea cause cognitive decline?

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According to a study, people who have obstructive sleep apnea may experience cognitive decline.

The study is distinctive because all of its subjects were in good health and were free of the comorbid conditions that are frequently cited as the processes behind the association between sleep apnea and cognition.

According to the study, males as young as middle age can experience cognitive decline brought on by obstructive sleep apnea.

When a person has obstructive sleep apnea (OSA), their airway occasionally becomes obstructed for at least 10 seconds while they are asleep. It has been hypothesised that the cardiovascular or metabolic comorbidities that cause these breathing disruptions are the cause of the eventual decline in cognitive function.

According to a recent research of individuals without these comorbidities, sleep apnea itself can cause cognitive deterioration as early as age 40.

Men from a distinctive group took part in the study. People with systemic hypertension, hyperlipidemia, diabetes, cardiovascular disease, and other metabolic illnesses are more likely to be diagnosed with OSA.

This study is the first to examine the cognitive impact of OSA in otherwise healthy and non-obese persons because none of the study participants had any such comorbidities.

In their otherwise healthy subjects, the researchers discovered that OSA was associated with worsened executive function, visuospatial memory, vigilance (sustained attention), psychomotor function, and impulsive control.

Obstructive sleep apnea

According to a recent examination of data from 16 countries, 425 million adult men and women between the ages of 30 and 69 have moderate-to-severe OSA, and 936 million have mild-to-severe OSA. One estimate places the number of Americans with the illness at 25 million.

Sleep apnea might be one of two forms. The brain is unable to regularly signal the breathing muscles in people with less common central sleep apnea. OSA is more prevalent.

The dilator muscles that normally maintain the soft palate at the back of the throat open during breathing malfunction in people with obstructive sleep apnea or enable the tongue to impede the airway. Respiration is halted until the affected individual gasps or snorts to reopen the airway and restore breathing, which frequently happens before they completely awaken.

The link between obstructive sleep apnea and cognitive decline

According to the study’s findings, males who had severe obstructive sleep apnea had deficiencies in:

  • Vigilance
  • executive ability
  • Visual recognition memory in the short term
  • esteem on a social and emotional level

These issues were present in the males with mild obstructive sleep apnea as well, though not to the same extent as the individuals with severe versions of the illness. In reality, they hardly ever outperformed the control group in a meaningful way.

Even though the majority of men with sleep apnea had medical comorbidities, the study’s participants had none, including cardiovascular disease, diabetes, chronic inflammation, or depression. The authors pointed out that earlier studies blamed concomitant illnesses rather than sleep apnea for cognitive deficiencies.

Ivana Rosenzweig, MD, Ph.D., FRCPsych, a sleep specialist and consultant neuropsychiatrist, and the study’s lead author, said in an email to Healthline that “in our small proof-of-concept cross-sectional study, we demonstrated cognitive deficits in male patients with obstructive sleep apnea, even without any comorbidities.” This is extremely relevant because the current prevailing theory holds that cognitive deficiencies in this age range may be caused by comorbidities connected to obstructive sleep apnea.“

Rosenzweig stated, “Our research demonstrates that sleep apnea is sufficient to initiate cognitive alterations. Since the majority of these patients were (otherwise) healthy males with this condition, the vast majority of them were consciously ignorant that they already had cognitive abnormalities detected by the extremely sensitive testing battery.

The following are some potential causes of the cognitive issues, according to the researchers:

  • sporadic low oxygen
  • high blood carbon dioxide levels
  • changes in the brain’s blood flow
  • fragmented sleep
  • Neuroinflammation

They stated that sleep apnea is a disorder that could be harmful.

Sleep apnea and dementia

The chance of developing dementia, including Alzheimer’s disease, may be considerably raised by sleep apnea. An assessment of research from 2022 found that it does not appear to raise the likelihood of acquiring vascular dementia.

Unfortunately, dementia can also cause sleep disruptions, according to Merrill. “Sleep disturbances increase dementia risk,” she said. As a result, your memory may eventually deteriorate to the point of dementia, which will make it harder for you to sleep. In this way, disturbed sleep can contribute to a downward spiral, making it even more crucial to recognize and address sleep problems during early and midlife adult development. Dementia affects sleep in several different ways, Merrill continued. “Dementia is a neurodegenerative illness, which means that brain cells begin to malfunction and die as time passes.

The brain’s sleep centres begin to malfunction when a person loses brain cells, making it harder for us to communicate with our bodies to stay asleep. Sleep is frequently broken up or even inverted, keeping patients awake all night before they fall asleep for the most of the day.

Merrill stated, “Ideally, sleep will be optimised years before the potential onset of dementia.” “With better sleep, we may be able to postpone the age at which dementia first manifests itself. To increase a person’s healthy life span as much as feasible, sleep quality should be improved.

The CDC recommends that those aged 61 to 64 receive seven to nine hours of sleep per night, while those aged 65 and over should aim for seven to eight hours.

Causes of OSA and cognitive damage

“Craniofacial and physiological particularities can be a risk factor for OSA — having a short chin, large tonsils, a large tongue, etc.,” said neuroscientist Dr. Nadia Gosselin from the University of Montreal in Canada, who was not involved in the study.

According to her, “these peculiarities increase a person’s risk of upper-airway obstruction during sleep.”

Although it is unclear how OSA causes cognitive loss, several of its fundamental characteristics, such as sleep disruption, intermittent hypoxemia, neuroinflammation, and oxidative stress, may be to blame.

According to Dr. Gosselin, OSA stops sleep from playing its part in memory consolidation, brain plasticity, and the elimination of cerebral metabolic waste by continuously fragmenting sleep.

She stated that systemic inflammation and blood-brain barrier disruption resulting in neuronal death are two more potential causes.

According to one study, the hippocampus and the entorhinal cortex, two areas of the brain that degrade quickly in Alzheimer’s disease, have higher levels of oxidative stress and inflammation.

How to treat sleep apnea

The good news is that OSA can frequently be treated by making small lifestyle adjustments, such eating better, working out more, and decreasing weight, she continued.

Through a range of therapy techniques, doctors can also assist patients in controlling OSA.

The CPAP machine, which uses continuous positive airway pressure to keep the airway open while you sleep, is the OSA technology that is used the most frequently. People with central sleep apnea may also be given medication, CPAP machines, or other breathing aids.

Other OSA therapies include oral mandibular advancement devices or dental appliances that prevent the tongue from obstructing the throat. Additionally, there are neurostimulation implants for OSA, and surgery can occasionally be beneficial.

REFERENCES:

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