Alzheimer's disease (AD) is a devastating neurodegenerative disorder that causes progressive cognitive decline. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Frontotemporal lobar degenerations are a group of disorders characterized by circumscribed degeneration of the frontal and temporal lobes and diverse histopathologic features. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Huntington's disease (HD) is an autosomal dominant, late onset, neurodegenerative disease characterized by motor deficits and dementia that is caused by expansion of a CAG repeat in the HD gene. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia with parkinsonism (FTDP) is a major neurodegenerative syndrome, particularly for those with symptoms beginning before age 65 years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We report a Japanese family with early onset hereditary frontotemporal dementia and a novel missense mutation (Ser305Asn) in the tau gene. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Exonic and intronic mutations in Tau cause neurodegenerative syndromes characterized by frontotemporal dementia and filamentous tau protein deposits. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Alzheimer's disease (AD) is the most common neurodegenerative cause of dementia and is responsible for significant individual morbidity and mortality, and economic impact on the health care system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found that these brain ApoE knock-out (bEKO) mice had synaptic loss and dysfunction similar to that of ApoE KO mice; however, the bEKO mice did not have the learning and memory impairment observed in ApoE KO mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Growing evidence suggests that soluble Aβ species can drive Alzheimer disease (AD) pathogenesis by inducing a cascade of events including tau hyperphosphorylation, proteasome impairment, and synaptic dysfunction. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a currently incurable neurodegenerative disorder and is the most common form of dementia in people over the age of 65 years. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A group of similar autosomal dominant hereditary neurodegenerative disorders have been linked to chromosome 17 in thirteen kindreds. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are characterized by hyperphosphorylation of the microtubule-associated protein tau and its accumulation into fibrillar aggregates. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Six tau isoforms differing in their affinity for microtubules are produced by alternative splicing from the MAPT (microtubule-associated protein tau) gene in adult human brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Estrogen is an important hormone signal that regulates multiple tissues and functions in the body. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of amyloid-beta (Abeta) into senile plaques in Alzheimer's disease (AD) is a hallmark neuropathological feature of the disorder, which likely contributes to alterations in neuronal structure and function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dysregulation of autophagy, a cellular catabolic mechanism essential for degradation of misfolded proteins, has been implicated in multiple neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The PS19 mouse model expressing the P301S tau mutation exhibits tau pathology associated with frontotemporal dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
HTT IAs carriers patients exhibited decreased survival after disease onset compared to non-carriers. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
33/100
Barnes Maze Acquisition was performed on males (N = 4-5/genotype) after habituation and several days training. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ABCA7-KO iMGs were deficient for proteins involved in lysosome function, measured by down-regulated lysosomal proteomic signatures, as well as reduced DQ-BSA activity and reduced LAMP1+ area. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E ε4 (APOE4) allele is the strongest genetic risk factor for developing sporadic Alzheimer’s disease (AD), which accounts for the vast majority of AD cases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is characterised by aberrant amyloid beta and tau aggregation, neuroinflammation, demyelination and neurodegeneration, which have been linked to changes in cell-specific gene expression signatures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →