The reasons for these differences remain unclear. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The reasons for these differences remain unclear. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Mechanisms underlying phenotypic heterogeneity in young onset Alzheimer disease (YOAD) are poorly understood. 1 key finding →
Participants: 37 Evidence: low
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Although we did not replicate the earlier association between the APOE 3-TOMM40 haplotypes and age at onset, we observed that the polyT polymorphism is associated with risk of LOAD in APOE 33 homozygotes in a large case-control series but in the opposite direction as in the previous study. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Discovery efforts for susceptibility loci for Alzheimer disease could benefit from the use of neuropathologic intermediate phenotypes as a complement to other approaches. 2 key findings →
Participants: 625 Evidence: low
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Cerebral amyloid beta (Aβ) deposition occurs in a substantial fraction of cognitively normal (CN) older individuals. 3 key findings →
Participants: 45 Evidence: low
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Missense mutations in two related genes, termed presenilin 1 (PS1) and presenilin 2 (PS2), cause dementia in a subset of early-onset familial Alzheimer's disease (FAD) pedigrees. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Converging evidence suggests that the accumulation of cerebral amyloid beta-protein (Abeta) in Alzheimer's disease (AD) reflects an imbalance between the production and degradation of this self-aggregating peptide. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid precursor protein (APP) gives rise to the amyloid-β peptide and thus has a key role in the pathogenesis of Alzheimer disease. 4 key findings →
Evidence: low
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In a recent preliminary study it was reported that a severe head injury resulted in the deposition of beta amyloid protein (beta AP) in the cortical ribbon of 30% of patients who survived for less than two weeks. 4 key findings →
Participants: 152 Evidence: low
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Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in nerve growth factor-differentiated PC12 cells increased apoptosis induced by trophic factor withdrawal or beta-amyloid. 4 key findings →
Evidence: low
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Temporal lobe epilepsy represents a major cause of drug-resistant epilepsy. 4 key findings →
Participants: 19 Evidence: low
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Evidence suggests interplay among the three major risk factors for Alzheimer's disease (AD): age, APOE genotype, and sex. 4 key findings →
Evidence: low
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Microglia are strongly implicated in the development and progression of Alzheimer's disease (AD), yet their impact on pathology and lifespan remains unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mechanisms underlying the protective effect of apolipoprotein E (APOE) ε2 against Alzheimer disease (AD) are not well understood. 4 key findings →
Participants: 982 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Sleep disturbances are frequent in AD. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The objective of this study was to analyze factors influencing the risk and timing of Alzheimer's disease (AD) in central Norway. 4 key findings →
Participants: 376 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Age and the apolipoprotein E ε4 allele are well-known risk factors for Alzheimer disease, but whether female sex is also a risk factor remains controversial. 4 key findings →
Design: longitudinal study Evidence: moderate
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Ageing of the brain leads to impairments in cognitive and motor skills, and is the major risk factor for several common neurological disorders such as Alzheimer disease (AD) and Parkinson disease (PD). 4 key findings →
Evidence: low
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• Low ALPS index was significantly associated with high risk of MCI, and the risk of MCI decreased linearly with a higher ALPS index • High ALPS index was dose-dependently associated with a decreased progression from MCI to AD • High ALPS index may delay the MCI onset approximately 3.8 years among CN participants and delay MCI progression to AD by approximately 3.5 years in MCI group • Aβ in choroid plexus, tau in part of the cortex and executive function were partially mediate ALPS-AD association We aimed to explore the association between ALPS index and both risks of MCI from cognitively normal (CN) and incident AD progressed from MCI, as well as potential mediating factors. 1 key finding →
Participants: 519 Evidence: moderate
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We have used restriction isotyping (restriction enzyme isoform genotyping) for rapid typing of common apolipoprotein E isoforms (E2, E3, E4). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From the 144 participants (56.3% female and 43.7% male, with a mean [standard deviation] age of 80.7 [7.7] years), 118 participants were available for final follow-up. 4 key findings →
Design: cohort study Participants: 144 Evidence: moderate
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Alzheimer's disease (AD) is the most common form of dementia. 2 key findings →
Design: meta-analysis Evidence: high
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This article discusses how distinct protein aggregates found in various neurodegenerative disorders appear to cause these conditions. 3 key findings →
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To facilitate clinical trials of disease-modifying therapies, plasma concentrations of Aβ species are good candidates for peripheral AD biomarkers, but studies to date have generated conflicting results. 5 key findings →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results highlight the efficacy of founder populations for AD genetic studies. 4 key findings →
Design: case-control Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 1,383 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 28,180 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →