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Researchers used a natural experiment in Wales, where the shingles vaccine was rolled out in a way that made people born just before a certain date eligible — and people born just after it not eligible — for reasons unrelated to their health. This allowed scientists to compare dementia rates between two very similar groups of people who differed mainly in whether they received the vaccine. The study tracked over 280,000 older adults for up to seven years.

People who received the shingles vaccine were about 20% less likely to be diagnosed with dementia over the following seven years compared to those who did not. The protective effect was particularly strong in women, who showed an even larger reduction in dementia risk. The finding was published in Nature Medicine, one of the most prestigious medical journals in the world.

The shingles vaccine (Shingrix) is already widely recommended for adults 50 and older to prevent the painful shingles rash and its complications. These findings suggest it may also help protect the brain — a potential bonus benefit that researchers are still working to understand. The vaccine is covered by Medicare for most adults. If your loved one hasn't had it, it's worth asking their doctor about it — not only because of this study, but because shingles itself can be serious.

Scientists don't yet fully understand why the shingles vaccine might protect against dementia. One leading theory is that the varicella-zoster virus (which causes both chickenpox and shingles) may trigger inflammation in the brain that contributes to Alzheimer's-related changes — and the vaccine prevents this. More research is needed to confirm whether this is the mechanism, and whether other vaccines might have similar effects.

Scientists at Cold Spring Harbor Laboratory investigated whether blocking an enzyme called PTP1B could help the brain's immune cells — called microglia — do a better job of cleaning up amyloid-beta plaques, the protein deposits that accumulate in Alzheimer's disease. PTP1B is interesting because it's already linked to diabetes and obesity, meaning existing drugs that target it may already exist.

When PTP1B was blocked in mouse models of Alzheimer's, the brain's immune cells became more active and better at clearing amyloid plaques. Memory and learning performance in the mice improved measurably. The finding suggests that this enzyme plays a role in suppressing the brain's natural plaque-clearing ability — and that releasing that suppression could be beneficial.

This is early-stage research in mice, so it is not yet a treatment for humans. However, it opens a new avenue worth watching — especially because drugs targeting PTP1B already exist for other conditions, which could accelerate the path to human trials. The researcher who led this study, Professor Nicholas Tonks, has a personal connection: his own mother had Alzheimer's.

This study was done entirely in mice. Results in animal models of Alzheimer's frequently do not translate to humans — this has been one of the most frustrating patterns in Alzheimer's research. Human trials would be needed to know whether PTP1B inhibition is safe and effective in people. That process typically takes many years.

Researchers investigated whether a protein called DDC (DOPA decarboxylase) — which plays a role in producing dopamine — could serve as a reliable marker in blood or spinal fluid to identify Parkinson's disease and Lewy Body Dementia. Both of these diseases involve the loss of dopamine-producing neurons, so DDC levels may change in detectable ways when the disease is present.

DDC levels in spinal fluid were significantly lower in people with Parkinson's and Lewy Body Dementia compared to healthy adults, and they were also lower in Parkinson's patients than in people with Alzheimer's — meaning DDC may help distinguish between these diseases, which are currently very difficult to tell apart. The findings were published in Nature Medicine.

Today, Parkinson's and especially Lewy Body Dementia are diagnosed based largely on symptoms — a process that can take years and frequently leads to misdiagnosis. A reliable biological marker like DDC could eventually allow for earlier, more accurate diagnosis through a blood or spinal fluid test, giving families answers sooner and opening earlier access to appropriate treatment.

This research still needs to be validated in larger groups of patients before DDC can be used as a clinical diagnostic test. The sample sizes in current studies are relatively small. Researchers also need to determine the most practical and least invasive way to measure DDC reliably — spinal fluid tests require a lumbar puncture, while blood-based tests would be far more accessible.

For 25 years, Northwestern University scientists have studied a rare group of adults over 80 called "SuperAgers" — people whose memory performs as well as healthy adults in their 50s. This study summarized two and a half decades of findings about what makes their brains different.

SuperAgers have more neurons in a key memory-related brain region called the entorhinal cortex — and those neurons are significantly larger than in typical older adults and even people with early-stage Alzheimer's. Their brains also show lower levels of Alzheimer's-related tau tangles, and in some cases appear to resist the buildup of amyloid plaques entirely. Interestingly, SuperAgers also tend to be highly social and maintain strong relationships throughout their lives.

The SuperAger findings reinforce several things families can act on now: staying socially connected, remaining physically active, and keeping mentally engaged appear to be associated with better brain health in old age. While not everyone can become a SuperAger — genetics play a role — these findings suggest that how we live across our whole lives shapes how our brains age.

Scientists don't yet fully understand whether SuperAgers' brains are different because of how they lived — or whether they were simply born with brains that are more resistant to aging. Disentangling nature from nurture in the aging brain is an ongoing challenge. Researchers are now studying whether interventions can help more people develop SuperAger-like brain resilience.

Scientists at Baylor College of Medicine investigated whether tubulin — a protein that forms the structural scaffolding inside brain cells — plays any role in controlling the behavior of tau (linked to Alzheimer's) and alpha-synuclein (linked to Parkinson's and Lewy Body Dementia). Both of these proteins can misfold and clump together into toxic deposits that damage neurons.

Tubulin actively interacts with both tau and alpha-synuclein and steers them away from toxic clumping, guiding them instead toward a healthy, functional state. The researchers found that when the cellular pool of tubulin is increased, the proteins behave less destructively. This flips the conventional understanding — rather than being a passive bystander in neurodegeneration, tubulin appears to be an active protector.

This finding opens a new theoretical treatment direction: rather than directly targeting tau or alpha-synuclein (which has been difficult), future therapies might work by boosting the amount of tubulin in brain cells. Since this mechanism appears relevant to both Alzheimer's and Parkinson's — and potentially Lewy Body Dementia — a single approach might one day benefit patients across multiple diseases.

This is laboratory research — the findings have not been tested in animals or humans yet. Translating the biology of tubulin interactions into a safe and effective drug is a long and uncertain process. Much more research is needed before any clinical application is possible.

A team from Rush University and colleagues studied nearly 2,000 older adults over many years, tracking their cognitive health alongside a detailed assessment of how mentally stimulating their lives had been — from childhood through old age. They measured access to books, libraries, and museums at age 12, intellectual engagement at midlife, and ongoing learning activities in older age.

People in the top 10% for lifelong cognitive enrichment had a 38% lower risk of developing Alzheimer's disease compared to those in the bottom 10%. They also developed Alzheimer's about five years later on average, and mild cognitive impairment about seven years later. Even among people whose brains showed significant amyloid and tau buildup at death, those with higher lifetime learning showed better cognitive function — suggesting that mental engagement can build resilience against the disease's physical changes.

The practical message is encouraging: staying mentally engaged across your entire life — not just in old age — appears to offer meaningful brain protection. Reading, learning new skills, learning a language, playing games, visiting museums — these activities appear to build what researchers call "cognitive reserve," a kind of buffer that helps the brain cope with the damage Alzheimer's causes. It is never too late to start, but it is most powerful when it begins early.

This study shows an association, not proof that mental stimulation directly prevents Alzheimer's. People who read more throughout their lives may also differ in other ways — diet, exercise, social connection — that contribute to better brain health. The findings relied on participants' memories of their early habits, which may not always be accurate.