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.

Patients with Alzheimer disease have reduced levels of sRAGE in plasma compared with patients with vascular dementia and controls. 2 key findings →

Design: cross-sectional Participants: 152 Evidence: low

A reasonably accurate, validated model has been produced, with clinical application through a scored point system, to assist clinicians, residents, and family members in defining good goals of care around end-of-life care. 1 key finding →

Design: cohort study Evidence: moderate

Segmented hippocampal volume in children and adolescents with posttraumatic stress disorder

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Biological psychiatry 2005-09-30

Future longitudinal studies with trauma control subjects and neuropsychological measures are indicated to further elucidate the relationship between hippocampus and behavioral abnormalities in young PTSD subjects. 3 key findings →

Design: longitudinal study Evidence: moderate

Mild Cognitive Impairment as a Clinical Entity and Treatment Target

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Archives of Neurology 2005-07-01

M ILD COGNITIVE i m p a i r m e n t (MCI) has been actively investigated for the past decade. , 2 The term was coined in the late 1980s by the New York University group to identify individuals who were not cognitively normal for age and yet did not have overt dementia, and their outcomes were described in an article examining predictors of dementia by Flicker et al in the early 1990s. Flicker et al characterized MCI as equivalent to a Global Deterioration Scale rating of 3 and found that a diagnostic approach combining a careful, structured interview and the appropriate neuropsychological tests can discriminate those individuals with MCI likely to experience cognitive deterioration from those with a benign prognosis. 2 key findings →

Design: longitudinal study Evidence: moderate

Benefits of fatty fish on dementia risk are stronger for those without APOE epsilon4

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurology 2005-11-01

In the Cardiovascular Health Cognition Study, consumption of fatty fish was associated with a reduced risk of dementia and Alzheimer disease for those without the APOE epsilon4 allele. 2 key findings →

Evidence: low

Our findings suggest that the onset of dementia-related syndromes may be initiated by repetitive cerebral concussions in professional football players. 5 key findings →

Evidence: low

Alzheimer disease (AD) and, to a lesser extent, dementia with Lewy bodies (DLB) showed more pronounced MTA. 3 key findings →

Participants: 39 Evidence: low

Like acetylcholinesterase, butyrylcholinesterase (BChE) inactivates the neurotransmitter acetylcholine (ACh) and is hence a viable therapeutic target in Alzheimer's disease, which is characterized by a cholinergic deficit. 4 key findings →

Evidence: low

Targeting BACE1 with siRNAs ameliorates Alzheimer disease neuropathology in a transgenic model

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Nature neuroscience 2005-08-28

In Alzheimer disease, increased beta-secretase (BACE1) activity has been associated with neurodegeneration and accumulation of amyloid precursor protein (APP) products. 3 key findings →

Evidence: low

fMRI evidence of compensatory mechanisms in older adults at genetic risk for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 2005-02-01

The results suggest that brain response differences are not due to poorer general memory abilities, differential atrophy, or brain response during control conditions, but instead appear to be directly influenced by APOE genotype. 4 key findings →

Evidence: low

Sex, apolipoprotein E epsilon 4 status, and hippocampal volume in mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Archives of neurology 2005-06-01

The APOE*E4 genotype status appears to have a greater deleterious effect on gross hippocampal pathology and memory performance in women than in men. 4 key findings →

Participants: 193 Evidence: low

DWI predicts future progression to Alzheimer disease in amnestic mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 2005-03-01

The authors assessed whether measures of hippocampal water diffusivity at baseline can predict future progression to Alzheimer disease (AD) in amnestic mild cognitive impairment (aMCI). 1 key finding →

Evidence: low

Association between blood pressure, white matter lesions, and atrophy of the medial temporal lobe

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 2005-01-01

Blood pressure and indicators of small-vessel disease in the brain may be associated with atrophy of structures affected by Alzheimer pathology. 4 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