Hippocampal atrophy rate has been correlated with cognitive decline and its genetic modifiers are still unclear. 2 key findings →
Design: longitudinal study Evidence: moderate
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.
We identified 11 loci-5 in H2-non-carriers and 6 in H2-carriers-although none of the MAPT haplotype-specific associations achieved genome-wide significance. 5 key findings →
Participants: 18,841 Evidence: low
Full summary, score breakdown and related studies → Original source
55/100
Extensive simulations demonstrated that the proposed approach not only provided accurate selection of single nucleotide polymorphisms (SNPs) with comparable or higher power but also robust control of false positives. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Variations in the human genome have been found to be an essential factor that affects susceptibility to Alzheimer's disease. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We propose a novel method to identify disease-related genetic variants enriched by imaging endophenotypes, which are the imaging traits associated with both genetic factors and disease status. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Two novel SNPs (rs465401 and rs460420), both near the ADAMTS1 gene on chromosome 21, showed genome-wide significant associations with CSF NFL. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
55/100
Mild-cognitive impairment (MCI) occurs in up to one-fifth of individuals over the age of 65, with approximately a third of MCI individuals converting to dementia in later life. 2 key findings →
Participants: 122 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent genetic progress allows the molecular diagnosis of young-onset dementia, including Alzheimer's disease (AD) and frontotemporal dementia (FTD). 2 key findings →
Participants: 52 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most frequent diagnosis of neurodegenerative dementia with early (≤65 years) and late (>65 years) onset ages in familial and sporadic patients. 2 key findings →
Participants: 1,148 Evidence: moderate
Full summary, score breakdown and related studies → Original source
55/100
Genetic risk modeling for dementia offers significant benefits, but studies based on real-world data, particularly for underrepresented populations, are limited. 3 key findings →
Participants: 610 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mutation screening revealed a novel probably pathogenic mutation (PSEN1 p.Leu232Phe). 3 key findings →
Participants: 450 Evidence: low
Full summary, score breakdown and related studies → Original source
The aim of this paper is to systematically evaluate a biased sampling issue associated with genome-wide association analysis (GWAS) of imaging phenotypes for most imaging genetic studies, including the Alzheimer's Disease Neuroimaging Initiative (ADNI). 3 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Levels of sociability are continuously distributed in the general population, and decreased sociability represents an early manifestation of several brain disorders. 5 key findings →
Participants: 342,461 Evidence: low
Full summary, score breakdown and related studies → Original source
54/100
We investigated which factors might explain the differences between the frequencies of brain β-amyloid (Aβ) deposition in Korean and European cognitively normal individuals (CNs). 1 key finding →
Participants: 434 Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies have reported that a rare nonsynonymous variant rs75932628-T in the TREM2 gene is associated with increased risk of Alzheimer's disease and Parkinson's disease (PD) in European-descended populations. 2 key findings →
Participants: 908 Evidence: moderate
Full summary, score breakdown and related studies → Original source
54/100
We identified 133 unique and shared metabolites associated with ADAD, TREM2, and sAD. 5 key findings →
Participants: 133 Evidence: low
Full summary, score breakdown and related studies → Original source
53/100
Progressive supranuclear palsy (PSP) is a movement disorder with prominent tau neuropathology. 2 key findings →
Participants: 1,114 Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide polygenic scores (GPS), which aggregate the effects of thousands of DNA variants from genome-wide association studies (GWAS), have the potential to make genetic predictions for individuals. 1 key finding →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Causes of the well-documented association between low levels of cognitive functioning and many adverse neuropsychiatric outcomes, poorer physical health and earlier death remain unknown. 4 key findings →
Participants: 112 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex disorder influenced by environmental and genetic factors. 1 key finding →
Participants: 10,922 Evidence: low
Full summary, score breakdown and related studies → Original source
CAG trinucleotide expansion is the molecular basis of Huntington's disease worldwide and is a highly sensitive and specific marker for inheritance of the disease mutation. 4 key findings →
Participants: 1,007 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated tau at threonine-181 (P-tau181) demonstrates promise as an accessible blood-based biomarker specific to Alzheimer's Disease (AD), with levels recently demonstrating high predictive accuracy for AD-relevant pathology. 2 key findings →
Participants: 1,153 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 37 SuperAgers (73% female, mean [standard deviation] 82.7 [2.8] years old) and 35 controls (54% female, 83.7 [4.3] years old) were included. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
Hippocampal subfield atrophy is a prime structural change in the brain, associated with cognitive aging and neurodegenerative diseases such as Alzheimer's disease. 3 key findings →
Participants: 1,086 Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical genetic diagnosis was achieved in 7 of 50 (14%) of the patients, with a further 8 patients (16%) found to have established risk factors which may have contributed to their EOD. 5 key findings →
Participants: 50 Evidence: moderate
Full summary, score breakdown and related studies → Original source
From across this tag
9 of the 346 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 9. The same 9 appear here every time.
- Identification of PSEN1 and PSEN2 gene mutations and variants in Turkish dementia patients
- Genetic insights in Alzheimer's disease
- Bridging the gap: Short structural variants in the genetics of anorexia nervosa
- Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) Trial: Genetic Resource for Precision Nutrition
- Identifying Genes Associated with Alzheimer's Disease Using Gene-Based Polygenic Risk Score
- A polygenic risk score predicts mosaic loss of chromosome Y in circulating blood cells
- Genetic studies of quantitative MCI and AD phenotypes in ADNI: Progress, opportunities, and plans
- Shared genes and pathways in dementia: Insights from genome-wide association studies
- Atrial Fibrillation Genetics Update: Toward Clinical Implementation
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 →