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.

High Resolution Image Download MS PowerPoint Slide The aggregation of α-synuclein is crucial to the development of Lewy body diseases, including Parkinson’s disease and dementia with Lewy bodies. 1 key finding →

Evidence: low

Epidemiological data show that both PD incidence rate and prevalence rate show a significant age-dependent growth trend [3]. 5 key findings →

Design: cross-sectional Evidence: low

Using raw data from the CFD and the GLMnet algorithm, we could accurately differentiate between DEM vs. HC with accuracies ranging up to 94.0%. 4 key findings →

Participants: 407 Evidence: low

Among 160 centenarians, 63.7% did not meet the PCFP criteria and were classified as having dementia. 5 key findings →

Evidence: low

Higher education was associated with higher initial cognitive status but faster decline. 5 key findings →

Participants: 353 Evidence: low

BackgroundSleep disturbances often precede motor symptoms in neurodegenerative diseases like Parkinson's disease (PD) and dementia with Lewy bodies (DLB). 4 key findings →

Evidence: low

Chronic cerebral hypoperfusion can lead to neuronal necrosis, trigger inflammatory responses, promote white matter damage, and ultimately result in cognitive impairment. 2 key findings →

Evidence: low

Accurate diagnosis of frontotemporal dementia (FTD) with right anterior temporal lobe (RATL) predominance remains challenging due to lack of clinical characterization, and standardized terminology. 4 key findings →

Evidence: low

Therapeutic Approaches and Potential Mechanisms of Small Extracellular Vesicles in Treating Vascular Dementia

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Cells 2025-03-11

Small extracellular vesicles (sEVs), including exosomes as a subtype, with a diameter typically less than 200 nm and originating from the endosomal system, are capable of transporting a diverse array of bioactive molecules, including proteins, nucleic acids, and lipids, thereby facilitating intercellular communication and modulating cellular functions. 1 key finding →

Evidence: low

The thematic analysis identified 12 themes: manifestations, sexual practices, impact, control, emotional formulations, beliefs in causes of hypersexuality and attributions, relationship with the partner, dealing with hypersexuality, coping with hypersexuality, self-image, stigma and professional help-seeking. 5 key findings →

Evidence: low

The drive for positive social interactions, or "social rewards", is an important motivator of human behaviour, conferring several adaptive benefits. 5 key findings →

Evidence: low

Multiplex connectomics reveal altered networks in frontotemporal dementia: A multisite study

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Network Neuroscience 2025-01-01

A network neuroscience perspective can significantly advance the understanding of neurodegenerative disorders, particularly frontotemporal dementia (FTD). 5 key findings →

Participants: 28 Evidence: moderate

We dissociated four key cognitive components underlying remote thinking: spontaneous associative thinking, inhibition of unoriginal responses, intentional remote associative thinking, and verbal initiation; and replicated them in three independent datasets. 5 key findings →

Evidence: low

Emerging evidence implicating glymphatic dysfunction contributes to the pathogenesis of frontotemporal dementia (FTD). 3 key findings →

Participants: 37 Evidence: low

could serve as potential biomarkers for NAFLD-associated mild cognitive impairment; 3) bacterial metabolic functions involved in sugar degradation and the breakdown of tryptophan and glutamate were downregulated and linked to CXCL13 plasma levels and neuroinflammation; 4) correlations between SCFA concentrations disappeared with liver disease and cognitive impairment. 3 key findings →

Evidence: low

Patients with hearing impairment presented slightly altered results on cognitive tests, typical of a mild cognitive impairment. 4 key findings →

Participants: 30 Evidence: low

Mild cognitive impairment progresses slowly and may be reversible, providing a window of opportunity for intervention before it progresses to Alzheimer's disease, at which point treatments, at best, ameliorate symptoms with little efficacy towards delaying disease progression. 2 key findings →

Evidence: high

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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.

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