Temporal lobe epilepsy represents a major cause of drug-resistant epilepsy. 4 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Temporal lobe epilepsy represents a major cause of drug-resistant epilepsy. 4 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Evidence suggests interplay among the three major risk factors for Alzheimer's disease (AD): age, APOE genotype, and sex. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
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Sleep disturbances are frequent in AD. 4 key findings →
Design: longitudinal study Evidence: moderate
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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
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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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Our results highlight the efficacy of founder populations for AD genetic studies. 4 key findings →
Design: case-control Evidence: moderate
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APP gene dosage is strongly associated with Alzheimer's disease (AD) pathogenesis. 3 key findings →
Evidence: preliminary
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This study reveals an important role of astrocytic apoE3 and apoE4 on the deposition and accumulation of Aβ plaques as well as on certain Aβ-associated downstream effects. 5 key findings →
Evidence: low
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We have previously shown that apolipoprotein E (Apoe) promotes the formation of amyloid in brain and that astrocyte-specific expression of APOE markedly affects the deposition of amyloid-beta peptides (Abeta) in a mouse model of Alzheimer disease. 1 key finding →
Evidence: low
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The impact of inflammation suppressor pathways on Alzheimer's disease (AD) evolution remains poorly understood. 2 key findings →
Evidence: low
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Polygenic risk scores have identified that genetic variants without genome-wide significance still add to the genetic risk of developing Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The ɛ4 allele of the apolipoprotein E gene (APOE), which translates to the APOE4 isoform, is the strongest genetic risk factor for late-onset Alzheimer disease (AD). 5 key findings →
Evidence: low
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Late-onset Alzheimer's disease (AD) is 50-70% heritable with complex genetic underpinnings. 4 key findings →
Participants: 104 Evidence: low
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Deposition of amyloid-β (Aβ) in the brain parenchyma and vessels is one of the hallmarks of Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hypometabolism in PiB-positive, cognitively normal subjects in a population-based cohort occurs in AD-signature cortical regions and to a lesser extent in other cortical regions. 4 key findings →
Design: cross-sectional Evidence: moderate
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The amyloid cascade hypothesis is widely accepted as the centerpiece of Alzheimer disease (AD) pathogenesis. 3 key findings →
Design: clinical trial Evidence: low
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10 of the 1,611 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 →