27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Directed conversion of mature human cells, as from fibroblasts to neurons, is of potential clinical utility for neurological disease modeling as well as cell therapeutics. 2 key findings →
Evidence: low
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These aggregated proteins contribute to the pathological and clinical heterogeneity of AD and are associated with a more rapid progression. 4 key findings →
Participants: 1,304 Evidence: low
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Alzheimer disease (AD) pathology begins 15–20 years before clinical symptoms, necessitating non - invasive biomarkers for early diagnosis. 4 key findings →
Participants: 120 Evidence: low
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Anti-amyloid immunotherapy is used to treat Alzheimer disease (AD) with moderate benefits and potentially serious side effects due to amyloid related imaging abnormality with effusions/edema (ARIA-E). 4 key findings →
Design: cross-sectional Evidence: low
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Mounting evidence suggests that defects in energy metabolism contribute to the pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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BackgroundAlzheimers disease (AD) is characterized by amyloid beta and tau accumulation accompanied by altered inflammatory responses. 4 key findings →
Design: cross-sectional Participants: 261 Evidence: moderate
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Hexanucleotide repeat expansions in C9orf72 are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, yet the predictive information contained within associated inflammatory and proteinopathy markers remains incompletely characterised. 1 key finding →
Evidence: low
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Human leukocyte antigen (HLA) class II variation is implicated in Alzheimers disease (AD) and longevity, but its mechanisms within the major histocompatibility complex remain unclear. 2 key findings →
Participants: 6,053 Evidence: moderate
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BackgroundUnderstanding the mechanisms underlying brain aging and age-related pathological changes is essential for advancing brain health research. 3 key findings →
Participants: 211 Evidence: moderate
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In female participants, higher education was associated with lower Thal amyloid phase, diffuse plaques, neuritic plaques, and Braak stage ({beta} range, -0.097 to -0.071; qFDR<.026); none was significant among male participants. 5 key findings →
Design: cohort study Participants: 2,592 Evidence: moderate
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Neuroinflammation is a principal driver of brain atrophy and cognitive decline in Alzheimers disease (AD). 2 key findings →
Participants: 49 Evidence: low
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ImportanceAnxiety phenotypes - rumination, global anxiety, and worry (RAW) - are increasingly associated with Alzheimers disease and related dementias (ADRD) risk, yet how anxiety phenotypes relate to coordinated, multi-system biology in the at-risk older adults is unknown. 4 key findings →
Design: longitudinal study Evidence: moderate
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We focus on neuroinflammation in disorders associated with frontotemporal lobar degeneration (FTLD). 5 key findings →
Evidence: low
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INTRODUCTIONAlzheimers, Lewy body and vascular neuropathology underpin the most common forms of dementia. 5 key findings →
Evidence: moderate
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Cellular mechanisms in early Alzheimers disease (AD) remain poorly understood despite generation of extensive observational multiomic data. 5 key findings →
Design: systematic review Evidence: high
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INTRODUCTIONInflammation plays a central role in Alzheimers Disease (AD), with oxylipins, endocannabinoids, and polyunsaturated fatty acids (PUFAs) acting as potent modulators. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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.
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 27,380 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.
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 →