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Scientists spot brain changes that may help predict stages of dementia

Scientists spot brain changes that may help predict stages of dementia

This is a significant and active area of research. Here’s a detailed breakdown of how scientists are spotting brain changes to predict the stages of dementia, moving from established methods to cutting-edge advances.

The Core Concept: Predicting Progression, Not Just Diagnosing

The key shift in modern dementia research is moving from a diagnosis based on clear symptoms to a predictive model. The goal is to identify the underlying disease process (like Alzheimer’s pathology) years or even decades before significant cognitive decline occurs, and then track its progression through predictable stages.

The most influential framework for this is the AT(N) Framework for Alzheimer’s disease, which classifies biomarkers into three categories:

  • A: Amyloid-beta pathology
  • T: Tau pathology
  • (N): Neurodegeneration or neuronal injury

Scientists use a combination of tools to measure these.


1. Key Brain Changes and the Tools to Spot Them

A. Amyloid-Beta Plaques (The “A” in AT(N))

  • What it is: Sticky protein fragments that clump together outside neurons, forming plaques. This is a hallmark of Alzheimer’s.
  • How it’s Spotted:
    • PET Scans (Amyloid-PET): A radioactive tracer binds to amyloid plaques in the brain, making them visible on a scan. A positive scan indicates amyloid accumulation, a key early risk factor.
    • Cerebrospinal Fluid (CSF) Analysis: A lumbar puncture can measure the levels of amyloid in the spinal fluid. Low levels of amyloid-42 in the CSF indicate that the protein is being trapped in the brain as plaques.

B. Tau Tangles (The “T” in AT(N))

  • What it is: Twisted fibers of a protein called tau that build up inside nerve cells, disrupting their transport system and eventually killing them. The spread of tau tangles is more closely correlated with the severity of cognitive decline.
  • How it’s Spotted:
    • PET Scans (Tau-PET): Newer tracers can now make tau tangles visible. This is a major breakthrough. Researchers can see where tau is building up and track its spread from memory centers to other brain regions, which predicts the transition from mild cognitive impairment (MCI) to full dementia.
    • CSF Analysis: Elevated levels of phosphorylated-tau (p-tau) in the spinal fluid are a direct marker of tau tangle pathology.

C. Brain Structure and Metabolism (The “N” in AT(N))

  • What it is: The downstream effects of amyloid and tau—actual brain cell death and loss of function.
  • How it’s Spotted:
    • MRI (Magnetic Resonance Imaging):
      • Volume Loss (Atrophy): MRI can precisely measure the shrinking of specific brain regions. In Alzheimer’s, early shrinkage is seen in the hippocampus and entorhinal cortex (critical for memory). The rate of atrophy can predict how quickly the disease will progress.
      • Connectivity: Advanced MRI can track the weakening of connections between different brain networks.
    • FDG-PET Scans: This scan measures glucose metabolism. Brain cells affected by dementia are less active and consume less sugar, showing up as “dark” or “cold” spots on the scan. A pattern of reduced metabolism in the parietal and temporal lobes is a classic predictor of Alzheimer’s progression.

D. A New Frontier: Blood-Based Biomarkers (Liquid Biopsy)

This is one of the most exciting recent developments. Scientists have developed highly sensitive blood tests that can detect minute levels of:

  • p-tau217 and p-tau181: These are specific forms of tau that are highly accurate in identifying Alzheimer’s pathology, even distinguishing it from other dementias.
  • Amyloid Ratios: Blood tests can now predict amyloid status in the brain with over 90% accuracy.

Why this is a game-changer: Blood tests are far cheaper, less invasive, and more scalable than PET scans or lumbar punctures, making them ideal for widespread screening and clinical trials.


2. How These Changes Map to Stages of Dementia

By combining these biomarkers, researchers can create a predictive timeline:

StageClinical PresentationKey Brain Changes (Biomarkers)
PreclinicalNo symptoms. The person functions normally.Amyloid begins to accumulate (positive Amyloid-PET or low CSF Aβ42). Tau may start to appear. This stage can last 10-20 years.
Mild Cognitive Impairment (MCI) due to Alzheimer’sMild, noticeable symptoms (e.g., forgetting recent conversations, getting lost), but not severe enough to interfere significantly with daily life.Tau spreads significantly, especially in memory regions. Neurodegeneration begins (hippocampal shrinkage on MRI, reduced metabolism on FDG-PET).
Dementia due to Alzheimer’sSignificant cognitive decline that impairs daily activities (managing finances, driving, personal care).Widespread tau pathology throughout the cortex. Significant and spreading brain atrophy. Marked hypometabolism.

The Future and Implications

  1. Early Intervention: The ultimate goal is to identify people in the preclinical or MCI stage and treat them with disease-modifying therapies (like lecanemab and donanemab) that clear amyloid or target tau, before widespread brain damage occurs.
  2. Personalized Prognosis: Doctors will be able to provide a more accurate prognosis by looking at an individual’s specific biomarker profile (e.g., “You have high amyloid and tau in region X, suggesting a higher risk of progression within 2 years”).
  3. Improved Clinical Trials: These biomarkers allow researchers to enroll the right participants for trials (those with the underlying pathology) and use biomarker changes as endpoints to see if a drug is working, much faster than waiting for cognitive scores to change.

Conclusion

Scientists are no longer just looking at a static picture of a “demented brain.” They are now using a dynamic toolkit of Amyloid-PET, Tau-PET, MRI, and blood tests to track the sequence of pathological events. This allows them to predict the risk, diagnose the specific stage, and forecast the likely progression of diseases like Alzheimer’s with ever-increasing precision, opening the door to a future where dementia can be slowed or prevented.

Reference:
https://www.medicalnewstoday.com/articles/brain-changes-blood-flow-metabolism-help-predict-alzheimers-stages-dementia
https://newsnetwork.mayoclinic.org/discussion/mayo-clinic-scientists-create-tool-to-predict-alzheimers-risk-years-before-symptoms-begin/
https://www.news-medical.net/news/20251110/New-diagnostic-approach-identifies-dementia-stages-based-on-neurovascular-and-metabolic-changes.aspx
https://www.sciencedirect.com/science/article/pii/S2274580725000238

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Psychedelics may ‘rewire’ brain to improve depression treatment: study

Psychedelics may ‘rewire’ brain to improve depression treatment: study

The Core Finding: “Rewiring” the Brain

The headline captures the essence of a significant shift in how scientists understand psychedelic therapy. The “rewiring” metaphor refers to the concept of neuroplasticity—the brain’s ability to form new neural connections and reorganize itself.

Traditional antidepressants (like SSRIs) work by gradually altering brain chemistry, primarily by increasing the levels of neurotransmitters like serotonin. Their effect is often described as “dampening” negative emotional responses.

Psychedelics like psilocybin (the active compound in “magic mushrooms”) appear to work differently and more rapidly. They don’t just modulate chemistry; they seem to induce a temporary state of heightened neuroplasticity. This means the brain becomes more flexible and open to change, potentially allowing it to break out of rigid, negative thought patterns associated with depression.


Breaking Down the Science: What the Studies Show

Several key studies have contributed to this “rewiring” theory:

  1. The “Reset” Hypothesis: Research using fMRI scans has shown that depression can cause the brain to fall into rigid, repetitive patterns of activity, particularly in a network called the Default Mode Network (DMN). The DMN is associated with self-referential thought, the “inner critic,” and mind-wandering. In depression, it’s often overactive.
    • What Psychedelics Do: Under the influence of psilocybin, the DMN temporarily breaks down or becomes less organized. This is thought to correlate with the subjective experience of “ego dissolution” or a loss of the rigid sense of self. When the DMN re-establishes itself, it may do so in a more flexible, less dominant way, effectively “resetting” this circuit.
  2. Growth of Neuronal Connections: Preclinical studies on animals have shown that psychedelics like psilocybin promote:
    • Dendritogenesis: The growth of new dendrites, the branch-like parts of neurons that receive signals.
    • Spinogenesis: The formation of new dendritic spines, the tiny protrusions where synapses (connections between neurons) are formed.
    • Increased Synaptogenesis: The creation of entirely new synapses.
      This literal physical “rewiring” increases the brain’s connectivity and computational capacity, potentially providing the hardware needed for new, healthier thought patterns to take root.
  3. The Role of Therapy (The Crucial Ingredient): The “rewiring” isn’t automatic. The psychedelic experience is often intense and can be challenging. The therapeutic context is critical. The drug-induced state of plasticity is paired with supported psychotherapy.
    • The therapist helps guide the patient through their experience.
    • In the following days and weeks, during the “plastic window,” the therapist helps the patient integrate their insights, process old traumas, and solidify new, healthier perspectives.

In essence, the psychedelic doesn’t cure depression on its own. It opens a critical window of opportunity where the brain is more receptive to change, and psychotherapy helps guide that change in a positive direction.


Key Takeaways and Implications

  • Rapid and Sustained Effect: Clinical trials have demonstrated that a single dose (or two) of psilocybin, when combined with therapy, can result in fast and significant reductions in depressive symptoms, with effects lasting for several months. This is a stark contrast to the weeks it can take for SSRIs to begin working.
  • Treatment-Resistant Depression: This approach shows immense promise for individuals who have not responded to conventional antidepressants, offering a new hope where other options have failed.
  • A Paradigm Shift in Psychiatry: This moves beyond the simple “chemical imbalance” model of depression towards a “circuit and plasticity” model. It focuses on the brain’s dynamic structure and its ability to heal itself.
  • Not a DIY Treatment: It is crucial to emphasize that this research is conducted in a strictly controlled medical setting. Self-medicating with psychedelics carries significant risks, including psychological distress and the potential to trigger latent mental health conditions.

The Road Ahead

While the results are promising, this is still an emerging field.

  • Larger-Scale Trials: More extensive Phase 3 clinical trials are underway to firmly establish efficacy and safety for regulatory approval.
  • Decriminalization vs. Medicalization: There’s an ongoing discussion about the legal and regulatory pathways, distinguishing between medical use and broader decriminalization.
  • Accessibility: If approved, a major challenge will be scaling this intensive, therapist-guided model to make it accessible and affordable.

In conclusion, the idea that psychedelics “rewire” the brain is a powerful and scientifically-grounded metaphor for a potentially revolutionary new approach to treating mental health disorders by harnessing the brain’s innate capacity for healing and change.

Reference:

https://www.medicalnewstoday.com/articles/psychedelics-may-rewire-memory-circuits-key-to-mental-health
https://www.ucsf.edu/news/2022/04/422606/psilocybin-rewires-brain-people-depression
https://pmc.ncbi.nlm.nih.gov/articles/PMC8209538

Medications that have been suggested by doctors worldwide are available on the link below
https://mygenericpharmacy.com/category/disease/mental-health

High levels of heart damage biomarker may signal increased dementia risk.

High levels of heart damage biomarker may signal increased dementia risk.

Recent research suggests that higher levels of certain heart-damage biomarkers may signal an increased risk of developing dementia later in life. I’ll walk you through what has been found, what it might mean, and what we don’t yet know. A large long-term study found that people aged approximately 45-69 who had higher mid-life levels of the cardiac biomarker High‑sensitivity cardiac troponin I (hs-troponin I), which signals subtle heart muscle injury, had a significantly higher risk of being diagnosed with dementia decades later.

Specifically, those with the highest troponin levels had about a 38% higher risk of dementia compared with the lowest troponin group. The elevated troponin levels showed up 7 to 25 years before the dementia diagnosis. In a subset of participants with brain MRI, higher troponin levels were associated with smaller hippocampal volume and less grey matter brain changes consistent with aging/degeneration.

More broadly, a review article notes that several cardiac biomarkers, including troponins, N‑terminal pro­ B‑type natriuretic peptide (NT-proBNP, a marker of cardiac/ventricular stress), and Growth‑differentiation factor 15 (GDF15, a marker of vascular stress), are associated with cognitive impairment or brain changes even in people without overt heart disease. A meta-analysis of coronary heart disease (CHD) found that people with CHD have a higher odds (~1.45 times) of developing cognitive impairment or dementia compared to those without CHD.

What it might mean — possible mechanisms
Here are some ways in which subtle heart damage / cardiovascular dysfunction might contribute to brain aging and dementia risk:
Reduced cerebral perfusion / heart-brain blood flow link: If the heart muscle is damaged (even subtly), cardiac output or the efficiency of circulation might decline, which could impair blood flow to the brain over the years. The brain is highly sensitive to its blood supply.

Vascular damage and micro-injuries: Biomarkers of cardiac injury or stress also correlate with vascular stress. This may manifest in the brain as white matter changes, microinfarcts, or reduced brain tissue volume (as found in the MRI subset).

Shared risk factors: Many heart injury markers are elevated in the presence of high blood pressure, diabetes, high cholesterol, obesity, smoking, etc. These risk factors also contribute to dementia. So part of the association may be explained by overlapping risk pathways.

Early warning / silent damage: The troponin elevations in the study were associated with “subclinical” heart damage (i.e., no overt symptomatic heart disease at baseline). That suggests damage begins much earlier than clinical diagnoses and may set the stage for brain aging for decades.

What we don’t yet caution:
These findings are observational in nature. That means we can’t yet say the elevated troponin caused the dementia, only that there’s an association. Indeed, the Mendelian-randomisation study found little evidence for a causal effect of genetically elevated cardiac biomarkers on dementia risk.

Exactly what threshold of troponin (or other biomarkers) is meaningful, and at what ages, is not yet firmly established. While plausible pathways exist (blood flow, microvascular injury, overlap of cardiovascular & cerebrovascular disease), the precise chain of events linking heart damage → brain injury → dementia remains under investigation.

Many of the studies focus on specific cohorts (e.g., the Whitehall II Study in the UK) and mostly middle-aged adults initially without heart disease. Whether the same associations hold in other populations, ethnicities, or older age groups is still being defined. If elevated cardiac biomarker levels identify a higher risk of dementia, we don’t yet have solid evidence that intervening specifically based on these biomarker levels (e.g., in addition to standard cardiovascular care) will reduce dementia risk.

Implications for health & prevention:
Mid-life heart health appears increasingly important for brain health in later life. What happens to the heart, vessels, and circulation may matter for the brain decades later. Monitoring cardiovascular risk factors (blood pressure, lipids, diabetes, smoking, obesity, physical activity) remains very important because these are modifiable and already known to influence dementia risk.

The idea of using cardiac biomarkers (like troponin) as part of a dementia risk assessment is emerging but not yet ready for routine clinical use solely for that purpose. For individuals, focusing on good cardiovascular health is also brain-health care. Eat healthy, exercise, manage weight/diabetes/hypertension, avoid smoking, and keep cholesterol/lipids in check. For clinicians/researchers: These findings may guide future work on early identification of who is at risk, and possibly on targeting brain-protective interventions earlier in those with evidence of silent cardiovascular damage.

Elevated levels of cardiac injury biomarkers (especially high-sensitivity troponin) measured in mid-life are associated with an increased risk of dementia many years later, potentially reflecting that silent heart damage is setting the stage for brain aging/neurovascular injury. While this doesn’t prove causation, it strengthens the notion that the heart-brain connection is significant and that protecting cardiovascular health may help reduce dementia risk. If you like, I can pull up the full study details (sample size, follow-up years, exact biomarker levels, cognitive outcomes) and we can discuss how strong the evidence is and what it might mean for clinical practice. Would you like that?

Additionally, scientists discovered that study participants with high levels of troponin between the ages of 45 and 69 experienced a quicker decline in their memory, thinking, and problem-solving abilities. These participants also tended to have a smaller hippocampus and lower gray matterTrusted Source brain volume, both of which are signs of dementia. Poor heart health in middle age puts people at increased risk of dementia in later life,

Damage to the brain seen in people with dementia accumulates slowly over the decades before symptoms develop. Control of risk factors common to both heart disease, stroke, and dementia in middle age, such as high blood pressure, may slow or even stop the development of dementia as well as cardiovascular disease. We now need to carry out studies to investigate how well troponin levels in the blood can predict future dementia risk. Our early results suggest that troponin could become an important component of a risk score to predict the future probability of dementia.

https://www.medicalnewstoday.com/articles/high-levels-troponin-heart-damage-biomarker-middle-age-increased-dementia-risk

Sugar Substitutes Not So Sweet for Brain Health

Sugar Substitutes Not So Sweet for Brain Health

The headline is primarily based on a 2022 study published in the journal BMJ Neurology, titled “Artificial sweeteners and risk of cardiovascular diseases: results of the French NutriNet-Santé cohort.” While the study’s main focus was cardiovascular health, it also included extensive data on cognitive decline.

Key Details of the Study:

  • Participants: Over 100,000 adults in France.
  • Method: Participants self-reported their dietary intake, including the types and amounts of artificial sweeteners they consumed. They were then followed for an average of nearly 8 years.
  • Cognitive Findings: The researchers analyzed the data and found that participants with a high intake of artificial sweeteners (specifically, an intake higher than the average for the top third of consumers) had a higher risk of developing cerebrovascular diseases (like stroke) and a higher risk of cognitive decline, specifically dementia.

The “62% faster decline” figure comes from the calculated hazard ratio for cognitive decline. It means that, compared to those who consumed little to no artificial sweeteners, the high-consumption group had a 62% higher risk of showing a faster decline in thinking and memory skills over the study period.

The 7 Sugar Substitutes Linked to the Decline

The study didn’t just look at “artificial sweeteners” as a monolith. It identified specific compounds. The primary culprits identified were:

  1. Aspartame (e.g., Equal, NutraSweet)
  2. Acesulfame Potassium (e.g., Ace-K, Sunett, Sweet One)
  3. Sucralose (e.g., Splenda)

These three were most strongly associated with the negative cognitive outcomes. The study also included data on:
4. Saccharin (e.g., Sweet’N Low)
5. Cyclamate (banned in the U.S. but used elsewhere)
6. Thaumatin
7. Neohesperidin Dihydrochalcone (Neohesperidin DC)

It’s important to note that the associations were strongest and most consistent for aspartame, acesulfame-K, and sucralose.

How Could Sweeteners Affect the Brain?

The study was observational, meaning it can show a correlation but cannot prove that artificial sweeteners cause the decline. However, scientists have proposed several plausible mechanisms:

  1. Vascular Damage: Artificial sweeteners have been linked to an increased risk of stroke and other cerebrovascular issues. Since brain health is heavily dependent on good blood flow, damaging blood vessels in the brain can directly impair cognitive function.
  2. Altering the Gut-Brain Axis: Sweeteners can change the composition of gut bacteria (the microbiome). An unhealthy gut microbiome can increase inflammation throughout the body, including the brain, and may interfere with the signaling pathways between the gut and the brain.
  3. Tricking the Brain: The intense sweetness without the expected calories may disrupt the brain’s reward pathways and its ability to regulate sugar and energy metabolism, potentially leading to insulin resistance in the brain, which is a known risk factor for dementia.
  4. Direct Neurotoxicity: Some laboratory studies (though not conclusively proven in humans) have suggested that certain compounds, like aspartame metabolites (phenylalanine and methanol), could have toxic effects on brain cells at very high doses.

Important Caveats and Context

Before you purge your pantry, consider these points:

  • Correlation is not Causation: It’s possible that people who consume large amounts of artificial sweeteners are already at a higher risk for cognitive decline for other reasons. For example, they might be using sweeteners to manage weight or diabetes, which are themselves risk factors. The researchers statistically adjusted for these factors, but it’s impossible to rule out all unknown variables.
  • Dose Matters: The negative effects were seen in the highest consumers. Occasional use in a diet soda or yogurt is very different from consuming multiple artificially sweetened products every day.
  • One Study Among Many: While this is a large, high-quality study, it’s not the only one. The scientific community is still debating this issue, and other studies have had mixed results.
  • The “Healthier User” Bias: Some critics argue that people who are already unhealthy are more likely to seek out “diet” products, which could skew the results.

What Should You Do?

  1. Practice Moderation: This is the golden rule. You do not need to panic, but it is wise to be mindful of your intake. Treat artificially sweetened foods and drinks as an occasional choice, not a daily staple.
  2. Read Labels: Start checking the ingredients lists on “sugar-free,” “diet,” and “zero-calorie” products. You’ll find these sweeteners in diet sodas, sugar-free candies and gums, flavored yogurts, protein bars, and even some brands of toothpaste and medicines.
  3. Consider Healthier Alternatives: If you want to reduce your sugar intake, consider focusing on whole foods and using small amounts of natural sweeteners. Options include:
    • Whole Fruit: Using mashed bananas, applesauce, or dates to sweeten baked goods.
    • Small amounts of Honey or Maple Syrup: While still sugar, they contain trace minerals and antioxidants.
    • Monk Fruit or Stevia: These are plant-based sweeteners that were not included in this particular study and are generally considered to have a better safety profile, though long-term data is still limited.

In summary, the headline is based on real and concerning scientific evidence. While more research is needed to establish a definitive cause-and-effect relationship, the prudent approach is to limit your consumption of artificial sweeteners, particularly aspartame, acesulfame-K, and sucralose, as part of a overall strategy for long-term brain and metabolic health.

Reference:

https://www.neurology.org/doi/10.1212/WNL.0000000000214023

https://www.medicalnewstoday.com/articles/7-sugar-substitutes-linked-62-faster-decline-thinking-memory-skills-aging

https://www.medscape.com/viewarticle/sugar-substitutes-not-so-sweet-brain-health-2025a1000nes

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Common sugar substitute may affect brain and blood vessel health.

Common sugar substitute may affect brain and blood vessel health.

Yes, recent research suggests that erythritol, a popular sugar substitute, may negatively impact brain and blood vessel health, increasing concerns about its long-term safety. Here’s what we know:

1. Link to Cardiovascular Risk

  • A 2023 study in Nature Medicine found that high blood levels of erythritol were associated with an increased risk of heart attack, stroke, and blood clot formation.
  • Erythritol appeared to enhance platelet clotting, potentially raising thrombosis risk, especially in people with existing heart disease or diabetes.
  • The study noted that even moderate consumption could lead to prolonged elevated blood erythritol levels.

2. Possible Effects on Brain Health

  • While direct human studies on erythritol and brain health are limited, animal studies suggest that artificial sweeteners (including erythritol) may:
    • Disrupt the blood-brain barrier, potentially increasing neuroinflammation.
    • Alter gut microbiota, which is linked to cognitive decline via the gut-brain axis.
  • Some researchers hypothesize that chronic sweetener use could affect insulin signaling in the brain, possibly influencing neurodegeneration (though more evidence is needed).

3. Who Should Be Cautious?

  • People with heart disease, diabetes, or clotting disorders may be at higher risk.
  • Those consuming keto or low-carb products (which often use erythritol) in large amounts.

4. What Are the Alternatives?

  • Stevia or monk fruit (natural, no-calorie options with fewer known risks).
  • Moderate sugar intake (better than artificial substitutes in some cases).
  • Fiber-rich sweeteners (like allulose or small amounts of honey/maple syrup).

While erythritol is generally recognized as safe (GRAS) by the FDA, emerging research suggests caution especially for high-risk individuals. More long-term studies are needed, but reducing dependence on artificial sweeteners may be wise.

Reference:

https://www.physiology.org/detail/news/2025/04/25/popular-sugar-substitute-may-harm-brain-and-heart-health?SSO=Y

https://www.healthandme.com/nutrition/chemicals-found-in-sugar-free-desserts-may-impair-brain-function-study-finds-article-151686747

https://www.medicalnewstoday.com/articles/common-sugar-substitute-may-affect-brain-and-blood-vessel-health

Medications that have been suggested by doctors worldwide are available on below link

https://mygenericpharmacy.com/category/blood-thinner

3 ways to slow down type 2 diabetes-related brain aging

3 ways to slow down type 2 diabetes-related brain aging

Type 2 diabetes can impact multiple organ systems, including the heart, kidneys, eyes, and even the brain. Additionally, scientists have found evidence that diabetes accelerates brain aging, which may raise the risk of Alzheimer’s. This podcast explores lifestyle interventions that may help slow the cognitive decline associated with diabetes. However, is there a way to prevent this, and if so, how?

Type 2 diabetes accounts for more than 95 percent of the estimated 422 million cases of diabetes that occurred globally in 2014. 783 million people worldwide are predicted to receive a diabetes diagnosis by 2045. Over time, type 2 diabetes can cause numerous serious complications, including infections, heart disease, pain and loss of feeling (due to damage to nerves), and vision loss. It is a chronic illness that can impact several organs in the body. Diabetes can also have a detrimental effect on the brain.

Through a variety of pathways, type 2 diabetes has been linked in studies to memory loss, cognitive decline, and an elevated risk of dementia and Alzheimer’s disease. The good news is that certain lifestyle modifications can either prevent or postpone type 2 diabetes. In this episode, we look at the results of two recent studies that provide clues about potential strategies to slow the aging process caused by diabetes. However, how precisely does type 2 diabetes contribute to accelerated brain aging, and how can we counteract accelerated brain aging caused by diabetes?

To answer these and other questions, MNT editors and co-hosts Yasemin Nicola Sakay and Maria Cohut spoke with Thomas (Tom) Barber, MD, an honorary consultant endocrinologist and associate professor at the University of Warwick in the United Kingdom. Barber has also appeared in two previous episodes of the In Conversation podcast: Can diet and exercise reverse prediabetes? and 100 Years of Insulin. You can listen to the entire episode below or on your preferred streaming service.

What to know about cognitive functioning

What to know about cognitive functioning

Cognitive functioning has an impact on people’s memory and thought processes. A decline in a person’s mental and physical responses to their surroundings may result from impairment in this area of brain health. The way the brain functions and shows up as behavior is known as cognitive functioning or cognition.

It plays a crucial role in sustaining daily functioning and brain activity. It controls people’s thoughts, behaviors, learning, and attention to their surroundings. This article looks at dementia, mild impairment, cognitive decline, normal brain function, how the brain functions, and strategies to enhance cognitive function.

Cognitive functioning is the capacity for thought, learning, and memory. The mental process of gaining knowledge and understanding through thought and senses, paying attention, learning through memory, making decisions, planning, reasoning, speaking, and being aware of one’s surroundings is referred to as cognition in research from 2023.

One of the hardest-working organs, the brain operates automatically when it is in good working order. One aspect of a person’s brain health is cognitive function. Other factors include: Motor function: Which controls movements, balance, and how people move. The ability to perceive and react to emotions is known as emotional function. People’s feelings and reactions to touch sensations are referred to as tactile function.

All areas of the brain work together, but each area has its responsibilities:
The upper part of the spinal cord, the brain stem, controls vital functions such as breathing.
The cerebellum helps with movement.
The upper part of the brain stem controls reflexes and voluntary movements.
The forebrain has a left and right hemisphere: the left helps with word formation, and the right helps with reasoning skills.
The frontal lobe helps with short-term memory storage.
The motor cortex in each frontal lobe helps plan movement.
The parietal lobe behind the frontal lobe supports reading.
The somatosensory cortex helps receive sensory information.
The occipital lobe processes images and links to memory.
The temporal lobe is responsible for receiving information through the ear.
The inner brain helps modify our response to things we perceive in our environment.
The hypothalamus governs important functions such as waking up and emotional responses.
The hippocampus sends memories to the correct hemisphere.

Research shows how the brain monitors intricate social relationships.

Research shows how the brain monitors intricate social relationships.

According to a recent study conducted by researchers at University College London (UCL), our brains use fundamental “building blocks” of information to track how people interact, allowing us to navigate complex social interactions. Researchers scanned the brains of participants playing a straightforward game with two opponents and a teammate to see how well their brains tracked information about the group of players. The study was published in Nature.

Instead of recording each player’s performance, the researchers discovered that certain brain regions would respond to particular interaction patterns, or “building blocks” of data that could be put together to comprehend what was happening. Being social beings, humans can maintain track of extremely intricate and dynamic social dynamics. This requires a tremendous amount of mental capacity to recall not only specific individuals but also the different connections among them.

Our brains must use heuristics, or mental shortcuts that speed up decision-making, to condense and simplify the abundance of information involved in a group social interaction in real-time. This system should minimize complexity while retaining flexibility and detail. According to this study, our brains seem to employ a set of fundamental “building blocks” that reflect essential elements of social interactions, which helps us quickly understand novel and challenging social situations.

The study’s team of researchers from UCL and the University of Oxford recorded the brain activity of 88 participants while they played a basic game using functional magnetic resonance imaging (fMRI). To respond to a question comparing the performances of various players, the study participants had to keep track of a series of data regarding their own, their partners, and their opponents’ performance during the scan. Dr. Wittmann clarified: We wanted to know if our brains would employ a “sequential” frame of reference, which tracks the information in the order it was received, or an “agent-centric” frame of reference, in which particular brain regions monitor each player’s performance. Although we discovered that people do both, our brains can condense all of this information into manageable chunks.

The researchers were able to identify particular brain activity patterns that corresponded to a few distinct “building blocks,” each of which represented a pattern of player interaction. One building block, for instance, recorded data on how well a participant and their partner were performing in comparison to the opposing team. An increase in brain activity associated with this building block was correlated with a greater performance gap between the two teams. These particular activity patterns were discovered in the prefrontal cortex, a region involved in social behavior and decision-making.

According to the researchers, these basic building blocks seem to reflect interaction patterns that are prevalent in a wide range of circumstances. Our brains are probably learning particular interaction patterns that we encounter repeatedly as we develop social skills in life, according to Dr. Wittmann. These patterns might be ingrained in our brains as building blocks that are put together and put back together to create our perception of any social situation.

Journal Reference:

https://mygenericpharmacy.com/category/products/disease/epilepsy

Epilepsy is a central nervous system (neurological) disorder in which brain activity becomes abnormal, causing seizures or periods of unusual behavior, sensations, and sometimes loss of awareness.

Although smoking shrinks the brain, stopping could stop additional loss.

Although smoking shrinks the brain, stopping could stop additional loss.

According to a recent study, cigarette smoking causes brain shrinkage, with the damage increasing with the amount of time and intensity of smoking. Alzheimer’s disease, dementia, and cognitive decline are all more likely to occur when brain volume is lost. While it cannot be stopped, quitting smoking can help slow down the shrinkage of the brain. The authors of the study advise smokers of any age to make stopping their habit a top priority. Researchers at Washington University School of Medicine in St. Louis have found that smoking cigarettes shrinks the brain. Washington, MO (WashUMed). Additionally linked to a higher risk of dementia, Alzheimer’s disease (AD), and cognitive impairment is brain shrinkage. The findings of the study demonstrate that stopping smoking at any moment prevented additional gray matter loss. But once shrinkage happens, the brain does not regain its initial mass. Smoking has long been known to be bad for the heart and lungs, but its effects on the brain have received less attention from researchers.

Leading the research team is Dr. Laura J., a senior author. The director of WashUMed’s Health and Behavior Research Center, Bierut, set out to close a knowledge gap about the negative effects of smoking. The results of the investigation were just released in Biological Psychiatry Global Open Science. According to earlier studies, smokers have a higher risk of dementia. An estimated 14% of Alzheimer’s cases are thought to be related to smoking. Disentangling behavioral and genetic variables is necessary to examine the relationship between brain shrinkage and cigarette smoking. Genetics can affect both brain shrinkage and the desire to smoke; according to the authors, genetics accounts for roughly half of an individual’s preference for smoking. The researchers took into account variables like brain volume and genetic susceptibility to smoking. They came to the conclusion that although smoking may be inherited, smoking is a major cause of brain shrinkage. The UK Biobank’s 2019 data releases are analyzed in this study. It included brain imaging data from 32,094 participants who were of European descent. The participants admitted to smoking on their own.

Researchers determined the number of years that smokers who reported consuming one pack or twenty cigarettes per day smoked cigarettes. Their brain images were contrasted with those of nonsmokers and smokers who had smoked less than 100 cigarettes. There was more brain shrinkage in those who smoked more. Dr. Neurons and their connections are lost in brain shrinkage, also known as atrophy, according to Dung Trinh of the Healthy Brain Clinic in Long Beach, California, who spoke with Medical News Today. Dr. Trinh did not work on the project. According to Dr. Trinh, this loss may affect the brain’s ability to operate properly. Dr. According to Trinh, certain crucial regions shrink in diseases like Alzheimer’s disease and dementia in general, which leads to a loss of function. For instance, he pointed out that Alzheimer’s patients frequently exhibit marked atrophy in the hippocampus, an area essential for memory formation. A decrease in cognitive function may arise from this atrophy’s suppression of interregional communication in the brain. Dr. Bierut made the observation that aging is linked to a decrease in brain volume. To put it another way, she claimed that smokers’ brains are “older”.

According to Dr. Bierut, smoking exposes oneself to numerous harmful chemicals. She continued by saying that smokers’ blood oxygen levels are consistently lower. According to Dr. Bierut, the brain is slowly starving itself because it loves oxygen and these prolonged low oxygen levels are starving it. Dr. Trinh enumerated a number of ways smoking can damage the brain. According to him, vascular damage can lower blood flow to the brain, which can cause atrophy and cell death. Dr. Trinh mentioned how smoking causes oxidative stress and inflammation, both of which can harm brain cells and the structures that support them. Cigarette smoke contains certain neurotoxic chemicals that can cause direct harm to brain tissue. According to Dr. Trinh, smoking alters the brain’s levels of several neurotransmitters, which over time may lead to atrophy and neural damage. According to Dr. Bierut, giving up smoking is among the most significant things you can do for your health. Your brain ages more quickly the longer and heavier you smoke. Additionally, I always tell older smokers that it’s never too late to give up. Even at a later age, quitting has health benefits.

In general, as the world’s population ages, a growing number of elderly people will experience dementia. This is a serious public health issue, and in order to have a healthy senior population, we must concentrate on lowering the modifiable risk factors for dementia. Dr. Trinh added that not only adults should give up smoking at the same time. Because the brains of teenagers and young adults are still developing, exposure to the negative effects of smoking during these formative years may result in more severe long-term damage, according to Dr. Trinh. It is a well-known fact that the potential lifetime harm from smoking increases with age. Dr. Robert Miller, an internal medicine physician with Vista Staffing, a company that provides physician search services nationwide, recommended a multimodal strategy for quitting smoking that includes counseling therapy. Dr. Miller did not work on the project. According to him, supportive pharmacotherapy and behavioral modification are the goals of this strategy. Dr. Miller listed seven drugs that have been given FDA approval to aid in quitting smoking, including nicotine replacement therapies (i.e. e. oral tablet medications (i.e., nicotine patches, lozenges, gum, oral inhaler, and nasal spray). e. , bupropion SR and varenicline).

According to Dr. Miller, helping others break the habit and finding success through a common goal can support each person on their own journey. It could also be beneficial to substitute healthy pursuits like reading or working out for the craving to smoke. According to Dr. Miller, some people discover that their urge to smoke might be a reaction to specific triggers. One way to kick the smoking habit is to recognize and stay away from personal triggers. It is not thought that vaping is a secure or reliable method of quitting smoking for those who are thinking about using e-cigarettes.

REFERENCES:

https://medicine.wustl.edu/news/smoking-causes-brain-shrinkage/
https://www.medicalnewstoday.com/articles/smoking-causes-brain-shrinkage-but-quitting-may-prevent-further-loss
https://www.mobidoctor.eu/blog/smoking-causes-brain-shrinkage-but-quitting-may-prevent-further-loss
https://www.mlo-online.com/disease/article/53081262/smoking-causes-brain-shrinkage
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In a period of 12 weeks, taking a fiber supplement may enhance cognitive function in older adults.

In a period of 12 weeks, taking a fiber supplement may enhance cognitive function in older adults.

The typical mild cognitive decline of aging can deteriorate due to diseases like dementia and Alzheimer’s disease. Currently, dementia and Alzheimer’s disease have no known cures. Elderly people’s brain function may be enhanced by dietary fiber supplements, according to research from King’s College London. Every bodily system, including the brain, slows down as we get older. In a healthy aging brain, it’s normal to experience difficulties with multitasking, word recognition, and name recall Source. The mild cognitive decline of an aging brain can sometimes worsen due to diseases like dementia and Alzheimer’s disease. More significant problems like memory loss, the inability to organize or solve problems, trouble speaking or writing, mood swings, anxiety, trouble sleeping, and confusion about locations, dates, and times can result from this. Even though there isn’t a cure for dementia or Alzheimer’s disease at this time, some medications and healthy lifestyle choices can help slow the disease’s progression. According to recent research, older adults’ cognitive function may be enhanced by dietary fiber supplements, according to King’s College London researchers. Additionally, researchers discovered that participants’ muscle strength was unaffected by the fiber supplements.

The world’s population is aging faster than in the past and people are living longer, according to the World Health Organization Source. Globally, there were approximately 1.4 billion adults 65 and older in 2022; by 2050, that number is predicted to rise to 2.1 billion. Senior author of this study Dr. Claire Steves, professor of aging and health and head of the Department of Twin Research and Genetic Epidemiology at King’s College London, told Medical News Today that new approaches to treat age-related conditions like cognitive decline are crucial given the global increase in aging. According to Dr. Steves, this leads to a rise in age-related illnesses, which significantly affect elderly people’s capacity to lead fulfilling lives on their own. Many age-related conditions currently have no effective treatment, so it is critical that we concentrate our efforts in this area. According to her, further research is necessary to increase our understanding of how to stop, slow, or even reverse age-related declines. Dr. Steves and her colleagues concentrated on two prebiotic supplements in this study: fructooligosaccharides (FOS), a plant-based carbohydrate, and dietary fiber inulin.

Recent studies have demonstrated a connection between our health and wellbeing and the bacteria in our stomachs, also referred to as the gut microbiome. The gut-brain axis—a link between these bacteria and the brain—has been demonstrated by studies. There have also been demonstrated links to the health of the muscles and other organs. According to Dr. Steves, “we decided to test whether improving gut microbial health with a prebiotic could improve brain and muscle function.”. We are aware that FOS and inulin are commercially available prebiotic supplements that are safe, affordable, and linked to a healthy gut flora. Another trial that examined inulin and FOS in a population of people residing in nursing homes also had an impact on us. She went on, “Those who took the inulin and FOS supplement showed improvements in hand grip strength, exhaustion levels, and overall measures of frailty.”. According to earlier research, inulin alters the gut microbiome, lessens neuroinflammation, and speeds up the healing process after traumatic brain injury.

According to studies on FOS, the supplement may help prevent Alzheimer’s by lowering beta-amyloid levels in the brain, as well as help with neuroinflammation reduction and memory enhancement. For this study, 36 pairs of twins older than 60 were enlisted by the researchers. For a duration of 12 weeks, one twin per pair was administered a daily dietary fiber supplement, whereas the other twin was given a placebo. Scientists used video, online surveys, and cognitive tests to keep an eye on study participants. In order to enhance muscle function, participants were also required to consume a protein supplement and engage in resistance training. Because the study was double-blind, neither the analysis team nor the participants knew which they had been given until the end of the investigation. At the end of the study, researchers discovered that the group taking a fiber supplement performed better on tests of brain function, such as the Paired Associates Learning test Source, an early indicator of Alzheimer’s disease, and tests of processing speed and reaction time.

Over a 12-week period, Dr. Steves stated, “We were pleasantly surprised to find that those who received the prebiotic supplement had an improvement in memory and thinking tests compared to the placebo.”. This study adds to the body of evidence supporting the known relationship between gut bacteria and brain function, and it holds great promise for future research aimed at preserving cognitive function and preventing age-related memory loss. She continued, “We have demonstrated that a basic, affordable, and easily available fiber supplement, which promotes the growth of beneficial bacteria in the gut, can actually influence brain function and memory test results.”. This encouraging outcome in just three months shows great potential for improving brain and memory function in our aging population. The supplement and placebo groups did not significantly differ in terms of muscle strength, according to the scientists. Dr. Segil acknowledged that he agreed with the study’s authors that, at this point, it is challenging to report improvements in cognition and for the study to have clinical significance. Even after reading the study, he said, “I like to say you are what you eat,” but sometimes “your brain is what you eat,” so it’s difficult to say that altering your diet will prevent aging, improve your muscles, and sharpen your mind.

However, there is a correlation between poor diet and high blood pressure, diabetes, and heart and cardiovascular risk factors. He continued, “There are definitely things that you shouldn’t eat; it’s harder to say what you should eat.” Despite this, I can’t say whether or not adding fiber will help. Dr. Segil stated that he would prefer blood tests to be conducted in conjunction with this study to observe any changes in participant albumin and sugar levels. He continued, “I would really like to see these tests repeated with some blood tests to give a doctor like myself more meaningful data, to see if these kinds of things change things in the blood.”. The next step would be to determine whether changes in the blood translate to changes in the brain. Richard and Rapozo both expressed interest in seeing similar studies done using prebiotic fiber from whole foods as opposed to supplements.

I would like readers to consider fiber as a component of a whole food approach, which means that it is one of the many nutrients and compounds that we require for a healthy gut. Discover which foods you enjoy and will consume are especially high in fiber: fruits, vegetables, beans, nuts, seeds, and whole grains, according to Richard. The general consensus is to aim for 25–35 grams of fiber per day. For instance, depending on the type of bean or pulse, 1/2 cup of beans may contain anywhere between 6 and 9 grams of fiber. To determine how much fiber you might be consuming each day, pull up a chart on the internet Source that lists the amounts of fiber in various foods, she advised. Antioxidants, vitamins, and minerals, as well as extra prebiotic fibers—two, rather than all four—are included in high-fiber whole foods, according to Rapozo. Prebiotic fiber-rich common vegetables include garlic, onion, leek, and shallot, as well as asparagus, beets, fennel, green peas, snow peas, corn, and cabbage. Legume foods such as kidney beans, soybeans, lentils, and chickpeas are excellent providers of prebiotics. Apples, nectarines, peaches, persimmons, watermelon, grapefruit, and pomegranates are examples of fruit sources. Oats, wheat, rye, and barley are examples of whole grains. Pistachio and cashew nuts are also rich in prebiotic fiber.

REFERENCES:

https://www.medicalnewstoday.com/articles/taking-daily-fiber-supplement-may-improve-older-adults-brain-function-12-weeks
https://medicalxpress.com/news/2024-03-daily-fiber-supplement-older-adults.html
https://www.worldhealth.net/news/daily-fiber-supplement-may-improve-brain-function-12-weeks/
https://www.psypost.org/diet-and-brain-health-fiber-supplement-improves-older-adults-cognitive-function-in-just-three-months/

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