Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Find studies

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are devastating neurodegenerative diseases that, despite the availability of symptomatic and modestly beneficial treatments, still lack therapies capable of halting disease progression. 5 key findings →

Evidence: low

Pathological TAR DNA-binding protein-43 (TDP-43) is a defining feature of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Alzheimer's disease (AD). 4 key findings →

Evidence: low

Tauopathies are neurodegenerative diseases characterized by pathological tau accumulation, leading to motor and neuropsychiatric symptoms. 1 key finding →

Evidence: low

Furthermore, we showed that phosphorylated tau accumulates within the endo-lysosomal system of the CHCHD10 V57E -expressing flies and mammalian cells. 3 key findings →

Evidence: low

This diet has been shown to improve cognitive function in patients with mild cognitive impairment, Alzheimer’s disease, vascular cognitive impairment, and vascular dementia. 4 key findings →

Design: narrative review Evidence: low

The Gut Microbiota as a Mediator Linking the MIND Diet to Alzheimer’s Disease

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Nutrients 2026-04-30

The Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet has emerged as a promising dietary pattern associated with reduced Alzheimer's disease (AD) risk, supported by growing evidence that both diet and the gut microbiota are modifiable contributors to disease development and progression. 1 key finding →

Evidence: low

Participant experiences and perceptions formed three themes: (1) aging accelerates PCDS progression, (2) PCDS threatening daily life, and (3) adapting to changes. 5 key findings →

Evidence: low

Participants described AI tools as potentially helpful for obtaining information, monitoring patients, managing medications and appointments, providing companionship, and conducting logistical tasks. 1 key finding →

Participants: 30 Evidence: low

Individuals with dementia were more likely to have staff or family members present at death, to receive documented decisions to shift to EOL care, have symptom assessments made the final week of life and prescription of injectables. 5 key findings →

Participants: 39 Evidence: low

There are significant opportunities for speech-language pathologists (SLPs) to play important roles in the primary and secondary prevention of Alzheimer's disease and related dementias (ADRD) beyond current practices. 2 key findings →

Evidence: low

Soluble phosphorylated tau has become a key biomarker for Alzheimer's disease pathology, yet further mechanistic studies are needed beyond observational investigations to clarify the relationship between soluble p-tau species and intracellular tau pathology. 4 key findings →

Evidence: low

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), particularly semaglutide, have demonstrated substantial efficacy for glycemic control and weight management and are increasingly prescribed across diverse populations. 4 key findings →

Design: narrative review Evidence: high

Per-Capita Food Availability and Global Dementia Burden Across Multiple Exposure Windows

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Nutrients 2026-08-18

Higher per-capita food availability was positively associated with dementia outcomes in minimally adjusted models, particularly for the 2005 exposure window, although these associations were substantially attenuated after full covariate adjustment. 4 key findings →

Evidence: low

Compared to those in rural areas, participants who resided in urban areas during young adulthood had lower late midlife ADI (β = -0.85, p < .05), and better executive function (β = 0.19), processing speed (β = 0.24), and verbal fluency (β = 0.30) (ps < .05) in older adulthood. 4 key findings →

Evidence: low

The NfL assay met analytical criteria, with precision demonstrating coefficients of variation <3% across runs, a lower limit of quantification of 3.10 pg/mL, linearity with <12% deviation, and <10% interference. 5 key findings →

Participants: 20 Evidence: low

Hierarchical linear regression was used to assess an incremental contribution of the set of inflammatory markers’ PRS to explaining VF variance compared to the null model. 5 key findings →

Participants: 135 Evidence: low

Dementia is a debilitating disease that leads to a gradual loss of memory and other cognitive abilities and tends to develop in people over 60 years of age. 2 key findings →

Evidence: low

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Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed