27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Familial multiple system tauopathy with presenile dementia (MSTD) is a neurodegenerative disease with an abundant filamentous tau protein pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
The finding that a GGGGCC (G4C2) hexanucleotide repeat expansion in the chromosome 9 ORF 72 (C9ORF72) gene is a common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) links ALS/FTD to a large group of unstable microsatellite diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We have previously reported a large Danish pedigree with autosomal dominant frontotemporal dementia (FTD) linked to chromosome 3 (FTD3). 2 key findings →
Evidence: low
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The cognitive profile was predominantly amnestic and was associated with multiple domains. 1 key finding →
Participants: 1,784 Evidence: moderate
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Amyloid-beta peptide (Abeta) seems to have a central role in the neuropathology of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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We review the genetic risk factors for late-onset Alzheimer's disease (AD) and their role in AD pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to increased Alzheimer's disease (AD) risk. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Haplodeficiency of the microglia gene TREM2 increases risk for late-onset Alzheimer's disease (AD) but the mechanisms remain uncertain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial innate immune receptor associated with a lethal form of early, progressive dementia, Nasu-Hakola disease, and with an increased risk of Alzheimer's disease. 4 key findings →
Evidence: low
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 genetically linked to the risk for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A causative association was recently demonstrated between homozygous TREM2 mutations and frontotemporal dementia (FTD)-like syndrome and between heterozygous TREM2 exon2 genetic variations and late-onset Alzheimer's disease (AD). 4 key findings →
Participants: 1,030 Evidence: low
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Reduction in hippocampal and amygdala volume measured via structural magnetic resonance imaging is an early marker of Alzheimer's disease (AD). 4 key findings →
Design: case-control study Evidence: moderate
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Although mutations within the TREM2 gene have been robustly associated with Alzheimer's disease, it is not known whether alterations in the regulation of this gene are also involved in pathogenesis. 3 key findings →
Design: meta-analysis Evidence: high
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Alzheimer's disease (AD) is associated with abnormal tau and amyloid-β accumulation in the brain, leading to neurofibrillary tangles, neuropil threads and extracellular amyloid-β plaques. 4 key findings →
Design: meta-analysis Evidence: high
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Reliable biomarkers of frontotemporal dementia (FTD) are currently lacking. 4 key findings →
Design: longitudinal study Participants: 20 Evidence: moderate
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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
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From clinically based series it has been proposed that, in homozygotes for the apolipoprotein E epsilon 4 (apoE epsilon 4) allele, Alzheimer's disease is almost inevitable by the age of 80. 4 key findings →
Participants: 638 Evidence: low
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Cross-ancestry sex-stratified analyses identified several loci with evidence of interaction (p 0.05). 5 key findings →
Design: meta-analysis Participants: 25,284 Evidence: high
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The study encompassed 479 723 participants (mean [SD] age, 56.5 [8.1] years; 260 730 females [54.4%]), including 271 690 in the YOD analyses and 334 939 in the LOD analyses. 5 key findings →
Design: cohort study Participants: 723 Evidence: moderate
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Here we show that the associations of 57 metabolites with dementia risk varied by APOE4 genotype or other AD/ADRD risk variants. 3 key findings →
Evidence: low
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The human metabolome reflects complex metabolic states affected by genetic and environmental factors. 5 key findings →
Participants: 23,000 Evidence: low
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We present a comprehensive global analysis of genetic variants associated with autosomal-dominant Alzheimer's disease (ADAD). 2 key findings →
Participants: 550 Evidence: low
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Poor oral health and genetic susceptibility have each been linked to dementia risk, but their joint effects and subtype-specific associations remain unclear. 5 key findings →
Design: cohort study Participants: 7,553 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Aging and age-related diseases share convergent pathways at the proteome level. 1 key finding →
Participants: 43,616 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 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 10. The same 10 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 →