27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
All indicators of atherosclerosis were associated with dementia (odds ratios ranging from 1.3 to 1.9) and its major subtypes Alzheimer's disease (odds ratios 1.3-1.8) and vascular dementia (odds ratios 1.9-3.2). 4 key findings →
Participants: 284 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Multiple system tauopathy with presenile dementia (MSTD) is an inherited disease caused by a (g) to (a) transition at position +3 in intron 10 of Tau. 1 key finding →
Design: longitudinal study Participants: 21 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Both the magnitude and the extent of brain activation during memory-activation tasks in regions affected by Alzheimer's disease, including the left hippocampal, parietal, and prefrontal regions, were greater among the carriers of the APOE epsilon4 allele than among the carriers of the APOE epsilon3 allele. 1 key finding →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our results suggest that the TREM2 p.R47H substitution is a risk factor for frontotemporal dementia and Parkinson's disease in addition to Alzheimer's disease. 4 key findings →
Participants: 609 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Several families have been reported with autosomal-dominant frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), genetically linked to chromosome 9p21. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) is a paralytic and usually fatal disorder caused by motor-neuron degeneration in the brain and spinal cord. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are associated with loss of nuclear transactive response DNA-binding protein 43 (TDP-43). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
For neuropsychology measures, we noted the earliest significant differences between mutation carriers and non-carriers 5 years before expected onset, when differences were significant for all measures except for tests of immediate recall and verbal fluency. 2 key findings →
Participants: 220 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hereditary frontotemporal dementia associated with mutations in the microtubule-associated protein tau gene (MAPT) is a protean disorder. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial surface receptor that triggers intracellular protein tyrosine phosphorylation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Apolipoprotein E ε4 allele (i.e. ApoE4) is the strongest genetic risk factor for sporadic Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 221 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Tau gene has been consistently associated with the risk of Parkinson disease in recent genome wide association studies. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebral small vessel disease is a major cause of stroke and dementia, but its genetic basis is incompletely understood. 4 key findings →
Participants: 42,310 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Much of the genetic basis for Alzheimer disease (AD) is unexplained. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
A total of 8870 cases of all-cause dementia were observed over a median 13.9-year follow-up. 5 key findings →
Design: cohort study Participants: 782 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Complaints of poor memory by older people, particularly when new, may be a realistic subjective appraisal of recent brain changes independent of observed cognitive decline. 2 key findings →
Design: cohort study Participants: 1,336 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In tandem with the ever-increasing aging population in low and middle-income countries, the burden of dementia is rising on the African continent. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
NfL in both serum and CSF has the potential to serve as a biomarker for clinical disease onset and has a prognostic value in genetic FTD. 1 key finding →
Design: case-control study Participants: 174 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Using hippocampal atrophy as a quantitative phenotype in a genome-wide scan, we have identified candidate risk genes for sporadic Alzheimer's disease that merit further investigation. 1 key finding →
Design: case-control study Participants: 381 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Most investigations have previously focused on highly selected cohorts with established AD-endophenotypes (CSF biomarkers, autopsy report, PET etc.), while data on cohorts with clinical assessment are currently lacking, especially in non-European populations. 2 key findings →
Participants: 234 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Researchers at the University of Pittsburgh developed a new plasma p-tau217 test (using a different antibody than existing commercial tests) and validated it in 363 people, including some with genetic early-onset Alzheimer's mutations and community-dwelling older adults. 4 key findings →
Design: cross-sectional Participants: 363 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Analyzing postmortem brain pathology from over 3,200 people plus biomarker data from more than 10,000 more, researchers found that people who inherit two copies of the APOE4 gene variant (about 2-3% of the population) develop Alzheimer's brain changes almost universally and on a predictable timeline starting around age 55, much like known single-gene forms of Alzheimer's. The authors argue this makes APOE4 homozygosity itself a genetic form of Alzheimer's disease rather than just a risk factor. 3 key findings →
Design: cohort Evidence: high
Full summary, score breakdown and related studies → Original source
This study asked whether the genes that raise Alzheimer's risk are the same genes that cause amyloid plaques to build up in the brain, and found they are not quite the same thing. 5 key findings →
Design: case-control Participants: 770 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A polygenic score (PGS) for Alzheimer's disease (AD) was derived recently from data on genome-wide significant loci in European ancestry populations. 4 key findings →
Design: cohort Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Comparison of probands with their unaffected spouses yielded odds ratios for AD of 9.9 (95% CI, 6.5 to 15.1) for head injury with loss of consciousness and 3.1 (2.3 to 4.0) for head injury without loss of consciousness. 3 key findings →
Participants: 2,233 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
9 of the 3,549 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.
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
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.
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 27,780 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →