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 Helpline800-272-390024 hours a day, 365 days a yearFree, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
988 Suicide & Crisis Lifeline98824/7Call 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) Helpline866-232-84849:00 am - 9:00 pm ET, seven days a weekLicensed 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.
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Find studies
Showing 1,551–1,575 of 1,593 studies · free to read · tagged Genetics(page 63 of 64)· 27,380 in the whole library·How the 0–100 score works
From OpenAlex; 12,859 studies have no institution on record and are not counted here.
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.
Esse artigo buscou abordar a Doença de Alzheimer de Início Precoce (DAIP) acerca do curso clínico, dos fatores predisponentes e do manejo, por meio de uma revisão de literatura, com ênfase na diferenciação entre DAIP e Doença de Alzheimer de Início Tardio (DAIT), incluindo artigos publicados entre 2015 e 2025, obtidos nas bases de dados “Alzheimer's Association”, “ScienceDirect”, “Cochrane” e “PubMed”, utilizando as palavras-chave “Alzheimer”, “early” e “on-set”, com o conectivo AND. 4 key findings →
✓ Peer-reviewedalzhub usefulness score 26 out of 100.·Arandu-UTIC.·2026-03-27
El objetivo de este trabajo es desarrollar un algoritmo de forrajeo de bacterias para el alineamiento múltiple de secuencias genéticas. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·Research Square·2026-08-03
Alzheimer's disease progresses heterogeneously across diverse cohorts, yet current predictive models fail to capture this complexity while remaining clinically interpretable. 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2025-12-17
Alzheimer’s disease manifests through heterogeneous progression patterns across diverse populations, yet current predictive models fail to capture this complexity while maintaining clinical interpretability. 4 key findings →
⚠ Retracted — do not rely on italzhub usefulness score 16 out of 100.·Cell·2011-08-01
Directed conversion of mature human cells, as from fibroblasts to neurons, is of potential clinical utility for neurological disease modeling as well as cell therapeutics. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-04-01
Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217. 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-09-08
We estimated associations of educational attainment and Alzheimer disease genetic risk with treatment initiation and incident dementia and compared GLP-1 receptor agonist initiators with initiators of non-sodium-glucose cotransporter 2 inhibitor second-line therapies, with a separate sodium-glucose cotransporter 2 inhibitor compa 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-21
Cognitive and behavioural impairment frequently accompanies motor decline in amyotrophic lateral sclerosis (ALS), with 15% of cases meeting the diagnostic criteria for frontotemporal dementia (FTD). 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-21
Structural variants (SVs) are a major source of genetic variation yet remain underexplored in healthy aging and neurodegenerative diseases. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-17
Genome-wide association studies (GWAS) typically represent Alzheimers disease (AD) risk loci by a single lead SNP, although the lead SNP may capture only part of the genetic variation at a locus. 3 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-17
Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-17
Genetic variation at the TMEM106B locus has been associated with Alzheimers disease (AD) and related neurodegenerative phenotypes, yet its haplotypic architecture remains incompletely resolved. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-22
Alzheimers disease (AD) is defined by progressive neurodegeneration, yet a substantial fraction of its genetic risk maps to non-neuronal processes. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-23
Examples include subpopulations of CD4+ T cells associated with inflammatory bowel disease, characterized by enrichment for a multi-cytokine phenotype and overlap with the naive NF-kB-activated, central memory, and effector memory CD4+ T subtypes, and subpopulations of microglia associated with Alzheimers disease, characterized by depletion of homeostatic programs and localization to the midtemporal gyrus, dorsolateral prefrontal cortex, and medial entorhinal cortex. 3 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-26
IntroductionNeuropsychiatric symptoms (NPS)--including aggression, psychosis, anxiety, apathy, and depression--affect up to 85% of individuals with Alzheimers disease (AD) and are among its most disabling and costly manifestations, accelerating cognitive and functional decline, institutionalization, mortality, and healthcare costs. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-27
Polygenic and proteomic risk scores are both proposed for pre-symptomatic stratification, yet the extent to which they provide overlapping or complementary information has not been measured across neurodegenerative disease. 3 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-28
Genome-wide genotypes were quality-controlled, imputed, functionally annotated (yielding 16,935 gene regions comprising 90,607 functional variants), and associated with latent EEG features using Bayesian reduced rank regression. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-09-03
BackgroundPhenotypic age acceleration (PhenoAgeAccel), derived from PhenoAge, and MetaboHealth are composite exposures of biological ageing and metabolic health associated with dementia-related outcomes. 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-09-04
Multi-trait QTL (xQTL) colocalization has shown great promises in identifying causal variants with shared genetic etiology across multiple molecular modalities, contexts, and complex diseases. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-09-04
INTRODUCTIONMultimodal biomarkers have transformed Alzheimers disease research, but the incremental contribution of each modality to predicting progression from mild cognitive impairment (MCI) remains unclear. 3 key findings →
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 tierup to 10 pts
Journal's citation recordup to 4 pts
Study designup to 12 pts
Strength of evidenceup to 5 pts
Peer-review validationup to 10 pts
How recentup to 5 pts
Sample sizeup to 4 pts
Effect reportedup to 3 pts
Studied in peopleup to 3 pts
Randomised / blindedup to 2 pts
Times citedup to 7 pts
Citations per yearup to 5 pts
Impact for its field and yearup to 6 pts
Cited by studies hereup to 6 pts
Still being citedup to 4 pts
Senior author's track recordup to 4 pts
Institution's track recordup to 3 pts
Multi-centre collaborationup to 3 pts
Indexed in PubMedup to 2 pts
Free to readup 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.