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.

APOE ε4 carriers share immune-related proteomic changes across neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Nature medicine 2025-07-15

The APOE ε4 genetic variant is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) and is increasingly being implicated in other neurodegenerative diseases. 3 key findings →

Evidence: low

ApoE Cascade Hypothesis in the pathogenesis of Alzheimer's disease and related dementias

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neuron 2022-03-16

The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). 5 key findings →

Evidence: low

High complement levels in astrocyte-derived exosomes of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Annals of neurology 2018-03-10

Astrocytes fulfill neuronal trophic roles normally, but are transformed in Alzheimer disease (AD) into A1-type reactive astrocytes that may destroy neurons through unknown mechanisms. 2 key findings →

Participants: 28 Evidence: low

Dementia diagnosis increasingly relies on blood-based biomarkers, yet their performance in diverse populations remains insufficiently characterized. 1 key finding →

Design: cross-sectional Participants: 605 Evidence: moderate

APOE epsilon4 genotype and longitudinal changes in cerebral blood flow in normal aging

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Archives of neurology 2010-01-01

Our findings suggest that APOE epsilon4-mediated risk for Alzheimer disease is associated with widespread decline in rCBF over time that precedes the onset of dementia. 3 key findings →

Design: longitudinal study Evidence: moderate

We systematically compared structural imaging patterns of advanced brain aging (ABA) in the general-population, herein defined as significant deviation from typical BA to those found in Alzheimer disease (AD). 5 key findings →

Participants: 2,705 Evidence: moderate

Association of olfactory dysfunction with risk for future Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Annals of neurology 2008-02-01

Although olfactory dysfunction is commonly associated with Parkinson's disease (PD), it is not known whether such dysfunction can predate the onset of clinical PD in a community-based population. 2 key findings →

Evidence: moderate

Our results show that TREM2 is responsible for an unexpectedly high number of dementia cases in our cohort, suggesting that this gene should be taken into account when mutations in other dementia genes are excluded. 4 key findings →

Evidence: moderate

In older adults, variable agreement between in vivo imaging and CERAD NP score was observed. 3 key findings →

Design: longitudinal study Evidence: moderate

Racial, ethnic, and cultural differences in dementia caregiving: review and analysis

✓ Peer-reviewed alzhub usefulness score 57 out of 100. The Gerontologist 1997-06-01

This study provides a review and analysis of the empirical research published since 1985 that has examined the impact of race, culture, and/or ethnicity on the dementia caregiving experience. 1 key finding →

Evidence: low

Despite lower dementia prevalence, Black participants with dementia had more dementia risk factors, as well as greater cognitive impairment and neuropsychiatric symptom severity than White participants. 1 key finding →

Participants: 5,700 Evidence: low

RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neuron 2013-10-01

A hexanucleotide GGGGCC repeat expansion in the noncoding region of the C9ORF72 gene is the most common genetic abnormality in familial and sporadic amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 1 key finding →

Evidence: low

Genetic control of human brain transcript expression in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. American journal of human genetics 2009-04-01

We recently surveyed the relationship between the human brain transcriptome and genome in a series of neuropathologically normal postmortem samples. 4 key findings →

Participants: 188 Evidence: moderate

Proteomics-based aging clocks in midlife or late-life and their associated risk of dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Communications Medicine 2025-08-14

We investigated whether a discrepancy between chronological and biological age in midlife and late-life is associated with cognition and dementia risk. 5 key findings →

Design: cohort study Participants: 11,758 Evidence: moderate

in 1997, the prevalence of Alzheimer's disease in the United States was 2.32 million (range: 1.09 to 4.58 million); of these individuals, 68% were female. 5 key findings →

Evidence: low

Midlife NAFLD shows associations with AD and accumulating vascular pathology, revealing potential pathways linking liver function to dementia. 2 key findings →

Participants: 1,706 Evidence: low

Controversies and priorities in amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The Lancet. Neurology 2013-03-01

Two decades after the discovery that 20% of familial amyotrophic lateral sclerosis (ALS) cases were linked to mutations in the superoxide dismutase-1 (SOD1) gene, a substantial proportion of the remainder of cases of familial ALS have now been traced to an expansion of the intronic hexanucleotide repeat sequence in C9orf72. 1 key finding →

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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.

1,034 records (3.7% 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