Lipid droplets are dynamic cellular organelles that store neutral lipids and coordinate metabolic and stress-response pathways. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Functional phenotypes (e.g., subcortical surface representation), which commonly arise in imaging genetic studies, have been used to detect putative genes for complexly inherited neuropsychiatric and neurodegenerative disorders. 2 key findings →
Participants: 708 Evidence: low
Full summary, score breakdown and related studies → Original source
Preclinical models of Alzheimer's disease (AD) suggest APOE modulates brain function in structures vulnerable to AD pathophysiology. 5 key findings →
Participants: 608 Evidence: low
Full summary, score breakdown and related studies → Original source
Gene-based PRS identified 389 genes with 164 of them not previously reported as AD-associated. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has multiple clinically and pathologically defined subtypes where the underlying causes of such heterogeneity are not well established. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified a novel mutation c.401_406delinsTCTAT; p.(Asp134Valfs*55) in exon 3 of TREM2 in an Alzheimer's disease patient also carrying the p.Arg62His TREM2 variant. 3 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering receptor expressed on myeloid cells 2 (TREM2) is a central regulator of microglial activity and loss-of-function coding variants are major risk factors for late onset Alzheimer's disease (LOAD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering receptor expressed on myeloid cells 2 (TREM2) is a cell surface transmembrane receptor from the TREM receptor family, predominantly expressed on the microglia in the central nervous system (CNS). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified a PSEN1 variant (p.Thr291Pro) in an individual presenting with pure SP at 30 years of age. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations of 3 causative genes, namely presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP), have been identified as the major causes of early-onset familial Alzheimer's disease (EOFAD). 5 key findings →
Participants: 32 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Dementia and cognitive disorders are major aging-associated pathologies. 4 key findings →
Participants: 68 Evidence: low
Full summary, score breakdown and related studies → Original source
Although Alzheimer's disease (AD) is a central nervous system disease and type 2 diabetes MELLITUS (T2DM) is a metabolic disorder, an increasing number of genetic epidemiological studies show clear link between AD and T2DM. 5 key findings →
Participants: 448 Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
Alzheimer's disease (AD) is the most common cause of dementia with advancing age as its strongest risk factor. 3 key findings →
Participants: 47 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrovascular dysfunction likely contributes causally to Alzheimer's disease (AD). 1 key finding →
Participants: 44 Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
When risk factor p-values were FDR-adjusted, diastolic blood pressure was significantly associated with mean perfusion. 5 key findings →
Participants: 330 Evidence: low
Full summary, score breakdown and related studies → Original source
We identified chemicals enriched for dementia pathways, suggesting broad classes of chemicals contribute to dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ApoE-4 was strongly associated with AD in this sample (allele frequency = 0.46 vs. 0.14 in controls, p < 0.000001). 5 key findings →
Participants: 679 Evidence: low
Full summary, score breakdown and related studies → Original source
An association between the 19q13.2 chromosomal region and Alzheimer's disease (AD) has been reported in AD families and for sporadic AD. 5 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
The mean age was 51 ± 12 years. Forty-two of the patients had OSAS. 5 key findings →
Participants: 73 Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes contribute to a variety of functions in the brain, including homeostasis, synapse formation, plasticity, and metabolism. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The progressive decrement of neuropsychological performance is associated with HVL long before the emergence of clinically overt symptoms. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid angiopathy (CAA) is a type of beta-amyloidosis that occurs in leptomeningeal and cortical vessels of the elderly. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The blood-brain barrier (BBB) represents a considerable obstacle to brain entry of the majority of drugs and thus severely restricts the therapy of many serious CNS diseases including brain tumours, brain HIV, Alzheimer and other neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
47/100
ABCA1 (ATP-binding cassette transporter A1) is a major regulator of cholesterol efflux and high density lipoprotein (HDL) metabolism. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The epsilon 4 allele of apolipoprotein E (apoE) is a major risk factor for Alzheimer disease, suggesting that apoE may directly influence neurons in the aging brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 3,521 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Familial Danish dementia: co-existence of Danish and Alzheimer amyloid subunits (ADan AND A{beta}) in the absence of compact plaques
- Amyloid-Related Imaging Abnormality (ARIA) Beyond the APOE-ε4 Allele
- Comprehensive analysis of APOE and selected proximate markers for late-onset Alzheimer's disease: patterns of linkage disequilibrium and disease/marker association
- Apolipoprotein E: risk factor for Alzheimer disease
- Xenogeneic skin transplantation promotes angiogenesis and tissue regeneration through activated Trem2+ macrophages
- The Panama Aging Research Initiative Longitudinal Study
- Amyloid, the presenilins and Alzheimer's disease
- Alzheimer's disease: a comprehensive review of epidemiology, risk factors, symptoms diagnosis, management, caregiving, advanced treatments and associated challenges
- GSN gene frameshift mutations in Alzheimer's disease
- Investigating the Causal Relationship between Neuroticism and Alzheimer’s Disease Using Mendelian Randomization and the Mediating Role of Modifiable Risk Factors
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 →