Shingles Vaccine Protects Against Dementia

A flagship study came out in Nature in 2025 that solidified a long observed finding, that the Shingles (Herpes Zoster) vaccine can protect against dementia.

Previous studies were classic observational cohort designs which can fail to show causation or account for confounding factors. This 2021 study found "a combined analysis estimated a 31% lower risk" and indicated the need for stronger research.

In comes the 2025 Nature study, this time a natural experiment arose:

To provide causal as opposed to correlational evidence, we take advantage of the fact that, in Wales, eligibility for the zoster vaccine was determined on the basis of an individual’s exact date of birth. Those born before 2 September 1933 were ineligible and remained ineligible for life, whereas those born on or after 2 September 1933 were eligible for at least 1 year to receive the vaccine.

The finding:

We show that receiving the zoster vaccine reduced the probability of a new dementia diagnosis over a follow-up period of 7 years by 3.5 percentage points (95% confidence interval (CI) = 0.6–7.1, P = 0.019), corresponding to a 20.0% (95% CI = 6.5–33.4) relative reduction. This protective effect was stronger among women than men.

Interestingly, the newer recombinant vaccines seem to be ever more effective than the live-attenuated vaccines (the ones tested in the Nature experiment), though more studies are in the pipeline to deepen this finding.

The mechanism for why the protective effect happens is still TBD, though some hypothesize that detrimental impact of getting Shingles on the brain may cause long term damage that leads to dementia.

Either way, the impacts seem clear, the Shingles vaccine seems like a must-get in a full range defense against dementia.

Does Socialisation Reduce Cognitive Decline? A New Study Says Yes

For people who don’t already have dementia, but are worried about it, learning about protective factors and risk factors for cognitive decline is one of the only steps you can take. A common piece of advice is to remain socially active, but does it really make a difference?

A new study [1] looked into this and found a very clear correlation between higher levels of social engagement and better cognitive performance.

Why Researching the Impact of Social Engagement is Difficult

Defining social engagement isn’t as easy as you might think. As a paper tackling this issue points out, researchers tend to use many different, overlapping terms. For example, social participation, social connectedness and community engagement are all used, and other studies may focus instead on social isolation. The paper points out that the subtle distinctions between these methods makes it difficult to interpret the evidence as a whole.

What the New Study Adds

The new research [1] used a composite measure called the Social Engagement Index, which covers specific things like whether you live with other people, whether you went out for fun in the past month, whether you visited friends or family, whether you’re married, employed and more. The idea is to cover many metrics of social engagement and use all of them to produce the final score.

They used data from the National Health and Aging Trends Study from 2011 to 2019, which covers Americans aged 65 or older enrolled in Medicare, and discounted anyone likely to have dementia at the start of the study. They found that higher social engagement (at baseline) was associated with a reduced decline in memory, orientation (i.e. what day is it? Who is the vice president?) and executive function. This was also incremental: the more engaged, the better the outcome.

Does Social Engagement Reduce Cognitive Decline?

The overall picture isn’t as clear as we might like. A “systematic review of reviews” covered this issue (section 4.1 for a summary) and despite emphasizing that low social engagement increases your risk, concluded that the data on the presumed protective effect is inconsistent. That said, the difference between a protective effect and avoiding an increase in risk seems more of a philosophical issue than a practical one.

As the new study also suggests, it certainly seems better to be socially engaged than to not be.

New Study Suggests Blood Pressure Variability is What Matters for Cognitive Decline

A new study has found a new insight on the relationship between blood pressure and cognitive decline. Since hypertension is a well-established – and controllable – risk factor for cognitive decline, scientists assumed that reducing it is the best strategy. But this seems to be missing a crucial piece of the puzzle.

The Problem: Mixed Results on Lowering Blood Pressure

The new paper points out that different studies disagree about the cognitive benefits of interventions to reduce blood pressure.  

The SPRINT-MIND study recruited people with hypertension but not diabetes. It found a reduced risk of mild cognitive impairment for people on a more intensive blood pressure reduction regimen, but no difference in probable dementia.

Conversely, the ACCORD-MIND trial focused on people with type 2 diabetes and included a similar comparison of a more intensive vs. less intensive blood pressure reduction regimen. In this case, though, there was no difference in cognitive function.

What the New Study Did

The new research [1] pooled data from both of these trials, and analyzed the data again at participant-level. The paper notes that blood pressure variability (BPV) is linked to both cardiovascular events and cognitive decline, and tends to be higher in people with diabetes.

To test whether this is the important factor, researchers looked at BPV between each visit in the original studies. The original researchers used varying cognitive tests, but the authors identified two essentially equivalent measures of psychomotor processing speed among them. They used these to compare results across both studies.

What They Found: Higher Variability, Greater Decline

People with more variability in their blood pressure saw greater cognitive decline over the study period. In particular, those in the highest third of BPV had a faster rate of decline than those in lower thirds. The relationship seemed to be linear: each 10% increment of BPV led to consistently higher levels of decline.

What the Study is Missing

The study only focused on one measure of cognitive decline, rather than a global score. All participants also had a high cardiovascular risk, so the results might not carry over to other populations.

 What Doctors Can Do

One thing the study suggests is optimizing drug selection and timing to reduce BPV where possible. Doctors can also try novel interventions specifically designed to bring down BPV.

🩸Can a Blood Test Tell How Fast Your Brain Is Aging?

What if a blood sample could reveal which parts of your body are aging the fastest, and even predict your risk of developing diseases years before symptoms appear? 🤔❓

A new study published by Stanford researchers analyzed blood plasma proteins with nearly 3,000 proteins across 44,498 UK Biobank participants for organ aging, and 7,000+ proteins in 60,542 individuals for cell-type-specific aging.

Using Machine Learning, the scientists figured out how much composite protein “signature” represented each organ and let the models assign biological ages to 11 organ systems and 40+ cell types.

😮 Turns out one-third of us have at least one organ that's aging dramatically faster or slower than the rest.

They discovered that aging is far from uniform. Instead, different cells and organs age at different rates, meaning two people of the same chronological age can have very different biological aging profiles, where 1 in 4 participants had multiple extremely aged or youthful organs; 20–25% showed accelerated aging in a single cell type, while 1–3% had >10 rapidly aging cell types.

In the study, they claim that cellular aging signatures were uniquely associated with disease status:

• 🧠Astrocytes (brain support cells): Extreme astrocyte aging demonstrated a 12.59-fold increased risk of incident Alzheimer’s disease (AD).

• 💪🏻Skeletal muscle cells: People with aged muscle cells had a 12.7× higher risk of amyotrophic lateral sclerosis (ALS), detectable three years before symptoms appear.

• 🫁 Respiratory cells: Smokers with aged lung epithelial cells faced 58% higher lung cancer risk than smoking alone would predict.

🍀Interestingly, new findings on Alzheimer’s disease offer hopeful news for carriers of the APOE4 gene that has long been linked to Alzheimer’s.

1. The predictive power of astrocyte aging (HR = 5.16) was comparable to APOE4 carrier status itself (HR = 5.30).

2. APOE4 gene + aged astrocytes three times higher risk compared to an average APOE carrier.

3. In contrast, APOE4 carriers with youthful astrocytes appeared to neutralise the genetic risk completely as none of their 23 APOE4/4 carriers developed Alzheimer's.

4. Youthful astrocytes reduced overall AD risk by over 60%

Side Note: ♀️ Women seemed to be more vulnerable to the harmful associations in both APOE4 gene and aged astrocyes.

🧬The researchers also identified an inverse pattern via biological age quantification from blood for the APOE gene variants:

• APOE4 → astrocytes age faster, macrophages age slower

• APOE2 (the protective variant) → the exact opposite: younger astrocytes, older macrophages

Together, these findings highlight a shift in how we understand aging. Chronological age is merely one measure, and this algorithm may provide a more precise picture of one's health trajectories by decoding cellular aging signatures from blood.

✨ Check out the these links for a deeper read:

1. More on the APOE Gene 🧬

2. Stanford Medicine Newsletter: Biological age of our organs and cell types within them predict our disease risk, longevity.

😴 Sleep Is More Than Just Rest: The Hidden Link Between Sleep Disorders and Dementia 💤

Most of us know that a bad night's sleep makes us feel tired, irritable, and unable to concentrate the next day. But growing scientific evidence suggests that POOR SLEEP may have much more serious long-term consequences, increasing the risk of developing dementia and Alzheimer's disease (AD).

Let's look at some meta-analyses, published seven years apart, provide compelling evidence linking sleep disorders with dementia.

In Shi et al., 2017 (247,000 people): With 18 longitudinal studies - consolidated that sleep disturbances are an independent risk factor, not merely an early symptom of dementia.

• Insomnia was mainly linked to a higher risk of AD.

• Obstructive Sleep Apnea (OSA) was associated with increased risk of all-cause dementia, AD, and vascular dementia (VasD).

❓However, evidence was limited, with most studies relying on self-reported sleep.

In Ungvari et al., 2025 : Analysed 39 studies

• Insomnia raises all-cause dementia risk by 36%, AD by 49%, and VasD by 59%.

• OSA raises risk by 33% in all-cause dementia and 45% in AD.

In Zhang et al., 2025 : Analysed 76 studies

• Excessive Daytime Sleepiness (EDS): +41% in all-cause and +85% in VasD

• Sleep-Related Movement Disorders: +153% VasD (showing restless legs/periodic limb movements are primarily vascular risk factors).

💊 Ungvari et al., 2025 raises the question of whether treating sleep disorders can mitigate dementia risk and states that it remains an important avenue for future research, particularly mentioning:

• CPAP (Continuous Positive Airway Pressure) for Obstructive Sleep Apnea (OSA).

  • Has been found to improve cognitive performance, particularly in executive function and memory

• Cognitive Behavioral Therapy for Insomnia (CBT-I)

🧠 Why might poor sleep affect the brain?

During deep sleep, the brain activates the glymphatic system, a specialised waste-clearance pathway that removes metabolic waste products, including amyloid-beta proteins associated with Alzheimer's disease.

Poor or fragmented sleep may reduce this nightly "brain cleaning" process, allowing harmful proteins to accumulate. Sleep disorders may also contribute through:

• 🫀 Reduced oxygen supply to the brain (particularly in sleep apnea)

• 🩸 Increased inflammation

• ❤️ Higher blood pressure and cardiovascular disease

• 🧠 Greater oxidative stress

• 🔄 Disruption of normal circadian rhythms

All of these factors have independently been linked to cognitive decline and neurodegeneration.

💡 A Note for Caution: Remember that these factors are links / associations and not a direct cause.

They are more of an INDICATOR of things that often go hand-in-hand and have have a bilateral relationship, for example: People with dementia may experience increased daytime sleepiness and cognitive impairment.

While improving sleep cannot guarantee prevention of dementia, taking sleep seriously may be one of the most accessible ways to protect brain health as we age.

• 🧠 Your brain works hard all day. Give it the sleep it needs to repair, recover, and protect itself for the future.

Does the MIND Diet Really Prevent Neurodegenerative Disease?

Diet gets a lot of attention when it comes to preventing neurodegenerative disease, because improving it is one of the few simple, preventative actions we can all take.

This is exactly what motivated some researchers to devise what’s called the “MIND” diet, which was specifically designed to protect against cognitive decline and neurodegenerative diseases. But does it really work?

Developing the MIND Diet

The full name of the MIND diet is the Mediterranean-DASH Diet Intervention for Neurodegenerative Delay. Combining elements from the popular Mediterranean diet and the blood pressure focused DASH diet, it also incorporates other foods that evidence suggests help with dementia.

Broadly, it suggests eating:

• Vegetables, especially leafy greens

• Berries

• Whole grains

• Beans and legumes

• Nuts

• Poultry

• Non-fried fish

• Extra virgin olive oil

Initial research scored participants on how well their diet matched the MIND diet, and found a link between MIND diet score and reduced cognitive decline with age.

Testing the MIND Diet

The same research group also tested how the MIND diet impacted Alzheimer’s risk. The methodology and cohort were basically the same – based in Chicago, n = 923, mainly white and non-Hispanic – except they used the participants’ annual Alzheimer’s assessment instead of their global cognitive score. As in the previous study, they compared the MIND diet with the Mediterranean and DASH diets.

The study suggested strong adherence to all of these diets reduced Alzheimer’s risk, but MIND outperformed the others for people who only partially followed the recommendations.  

However, a randomized controlled trial of the MIND diet came to a conflicting conclusion. The test pitted the MIND diet against a control diet (n = 604) with a mild calorie restriction, and found that both diets improved global cognition scores. People following MIND scored a little better, but the difference wasn’t statistically significant.

Does the MIND Diet Really Work?

The best answer to this question comes from a meta-analysis focusing on dementia in general . The authors combined three studies for a cohort analysis (n = 18,136) and 11 studies for the meta-analysis (n = 224,049). Both analyses found that the mind diet is associated with lower dementia risk in older adults.

More evidence is still needed – especially for non-Western populations and specific types of dementia – but overall, it does seem effective.

🫚 Ginseng for Alzheimer's and Parkinson's ?!! 🧠✨

Chinese Medicine has been passed down for thousands of years, but only recently are we really analysing the ancient wisdom, and there seem to be some truth to them. 🧐

Ginseng, in particular, was long hailed as a miracle medicine that could save people who were close to death’s door. Well, research has found that Ginseng could work for two of the most devastating degenerative diseases: Alzheimer’s and Parkinson’s disease.

Although Alzheimer's and Parkinson's disease manifests very differently, one with physical ailments and the other in mental state.

They actually share several underlying pathological mechanisms 🧬, including oxidative stress, chronic neuroinflammation, mitochondrial dysfunction, and programmed cell death (apoptosis) 💀.

A meta‑analysis published by Pharmacological Research reviewed & confirmed that ginsenosides, the main bioactive compounds in ginseng, can deliver powerful neuroprotective effects and show great promise as a new therapeutic option.

Ginsenosides have been reported to:

• Stop toxic proteins (amyloid‑beta, tau, alpha‑synuclein) from clumping and damaging the brain cells

• Lower chronic brain inflammation, a major driver of cell death

• Boost antioxidant defence and reduce oxidative stress

• Protect neurons, improve signal transmission, and even support the growth of new brain cells

Unlike single‑target drugs that have not been of much use, researches contemplate whether the effectiveness seen in ginsenosides work because they target multiple pathways at once, which may have been necessary to curb these complex diseases.

Specifically:

• Rg1 stands out for boosting cognition and memory

• Rb1 offers neuroprotection by stopping harmful protein tangles

• Rare ginsenosides like Rg3, Rh2, and Compound K are even more exciting: formed through metabolism or special processing, they are absorbed better and show stronger protective effects than the more common forms.

While more human clinical trials are needed, the science is becoming increasingly difficult to ignore. An herb once praised in ancient texts for preserving vitality is now attracting serious attention from neuroscientists worldwide.

GLP-1s, Dementia, Alzheimer's, and Type 3 Diabetes

The suite of new GLP-1 agonists (GLP-1RAs) have shown a cascade of fascinating impacts, but the one that I have my eye on is this new idea that GLP-1 drugs may be preventative of brain aging diseases like Alzheimer's and Dementia.

GLP-1 is a naturally produced hormone in the human gut that regulates appetite and insulin secretion. The GLP-1 agonists drugs that have made a splash the last few years like semaglutide (Ozempic/Wegovy), liraglutide (Victoza/Saxenda), and dulaglutide (Trulicity), were originally developed for type 2 diabetes management.

But a 2026 Systematic Review found:

This study contributes to the clinical understanding of GLP-1 RAs and their effect on cognitive dysfunction. Findings from this study indicate GLP-1 RAs as potential therapeutics targeting cognitive function and neurocognitive disorders in persons living with T2DM.

This finding was echoed by a 2025 review which stated:

preclinical evidence has consistently shown the neuroprotective effects of GLP-1RAs, including reduced amyloid and tau pathology, improved synaptic function and enhanced neuronal survival

And a 2025 meta-analysis found that:

(GLP-1RAs) were associated with a statistically significant reduction in dementia

This finding was paired with a null result for the alternative cardio-protective glucose lowering agent sodium-glucose cotransporter-2 inhibitors (SGLT2is), suggesting the the GLP-1RAs are either using a unique pathway or are simply more effective. Contradictorily, a read world study released on the same day found benefits for both GLP-1RAs and SGLT2is; the meta-analysis may have been underpowered to detect SGLTis' benefits.

The link between Alzheimer's or Dementia and Diabetes is well known, with diabetes cited as a major risk factor. This is important to remember when contextualizing these findings as the population for the studies were almost all individuals with Type 2 Diabetes. That means we don't know if these neuroprotective effects can be generalized to people without T2D.

Interestingly as pointed out by the 2025 review, Alzheimer's and Dementia may be thought of as Type 3 Diabetes, as these diseases may be symptoms of underlying insulin dysregulation in the brain and damaged blood vessels. The tie between dementia and cardiovascular health echoes what we've heard in the past, that what's good for the heart is good for the brain. GLP-1 is naturally boosted by exercise and may point to the same correlation we see with exercise and brain health.

Excited to see how these findings pan out over the next few years, GLP-1RAs still require long term trials and reviews against the general population. The results for major trial targeting adults with early onset Alzheimer's released in March 2026 failed to show efficacy of oral semaglutide in reducing Alzheimer's. Note this study was funded by Novo Nordisk.

Oral semaglutide was not efficacious in slowing clinical progression in participants with early Alzheimer's disease.

This could be due to several reasons like the drug being more preventative than capable of reversing symptoms, weaker impacts of older generation GLP-1RAs or effects not being generalized outside of TD2 patients. But this is the strongest clinical result yet and points to the need for more trials before comprehensively marking success.

Social Determinants of Dementia: The Causes of the Causes

There are lots of risk factors for neurodegenerative diseases like dementia – like smoking, high blood pressure and obesity – but much less attention is paid to social factors liked to these diseases. But as a recent paper points out, they are essential when it comes to preventing dementia.

Social Determinants of Health in General

A social determinant of health is a way to think about the links between people’s health and how they live, work, study and socialize.

For example, low socioeconomic status (SES) is not likely to directly cause illness. However, it would impact the quality of care you receive, the things you’re exposed in your day-to-day life and even the type of work you do.

The social determinants of a condition can be thought of as “the causes of the causes” of illness.

The Social Determinants of Dementia – Reviewing the Evidence

The recent paper [1] looked at systematic reviews on the social and environmental determinants of dementia published between 2004 and 2024. The authors found strong evidence linking pollution and other environmental exposures to dementia.

Additionally, higher SES, higher education and higher social engagement had a protective effect, while lower SES and problems accessing healthcare were linked to increased risk.

The State of the Evidence

While I can’t get full access to the new paper, a study from last year covers the same ground. They looked at 100 papers, 26 systematic reviews and 74 primary studies, and found links for:

• Physical environment: 10 reviews and 15 primary studies looked at this. They conclude that air pollution is a factor, and likely mediates racial differences in dementia risk. Specifically, research suggests that your proximity to roads, how deprived your neighbourhood is, exposure to aluminium, pesticides, and solvents are linked to higher risk. Urban green space could help, but results are mixed .

• SES and work: 16 reviews looked at these issues. They found links with lower SES in general, and specifically for income and career success. Shift work, solvents, and (oddly) magnetic field exposure also showed a link. 

• Ethnicities and identity: Being black (relative to white) in the US, being Malay or Indian (in Asia-Pacific) and being indigenous (relative to white Australian) in Australia, and being a migrant vs. a native (in Europe) were linked to greater risk.

The authors point out that most evidence comes from high income countries, and studies from other countries would help to clarify the picture in key areas.

Happy to join this Board! My great-grandma and grandma had dementia, which makes me worry about my parents. Looking forward to learning together.