27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The distribution of apolipoprotein E (APOE) genotypes as a function of age and sex has been examined in a French population of 417 Alzheimer disease (AD) patients and 1,030 control subjects. 1 key finding →
Evidence: low
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Apolipoprotein E (apoE) plays a role in the pathogenesis of Alzheimer disease (AD). 5 key findings →
Evidence: low
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There is increasing evidence for blood-brain barrier (BBB) compromise in Alzheimer disease (AD). 5 key findings →
Evidence: low
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The amyloid beta protein and the amyloid beta-protein precursor (APP) are major constituents of senile plaques and cerebrovascular deposits in patients with Alzheimer disease and Down syndrome. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Immunostaining of adenosine receptors in the hippocampus and cerebral cortex from necropsies of Alzheimer disease (AD) patients shows that there is a change in the pattern of expression and a redistribution of receptors in these brain areas when compared with samples from controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease, the most common neurodegenerative disorder of senile dementia, is characterized by two major morpho-pathological hallmarks. 4 key findings →
Evidence: low
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The subcellular localization of organelles, mRNAs and proteins is particularly challenging in neurons. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Beta-site Amyloid precursor protein Cleaving Enzyme 1 (BACE1) is conceived as a potential target for therapies against Alzheimer disease (AD) which is characterized by the accumulation of plaques formed of short β-amyloid (APPβ) peptides. 4 key findings →
Evidence: low
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Autism is characterized by restricted, repetitive behaviors and impairment in socialization and communication. 4 key findings →
Evidence: low
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The control of viral infections in the brain involves the activation of microglial cells, the macrophages of the brain that are constantly surveying the central nervous system, and the production of amyloid-beta (Aβ) as an anti-microbial molecule. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most prevalent dementia, affecting a large number of populations. 4 key findings →
Evidence: low
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Cytoskeletal abnormalities and synaptic loss, typical of both familial and sporadic Alzheimer disease (AD), are induced by diverse stresses such as neuroinflammation, oxidative stress, and energetic stress, each of which may be initiated or enhanced by proinflammatory cytokines or amyloid-β (Aβ) peptides. 4 key findings →
Evidence: low
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Residence in the most disadvantaged neighborhoods may be associated with lower amyloid pathology in cognitively impaired individuals. 4 key findings →
Evidence: low
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Apolipoprotein E (ApoE) polymorphism has been appreciated as a valuable predictor of Alzheimer disease (AD), and the associated ε4 allele has been recognized as an indicator of susceptibility to this disease. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Environmental factors like neighborhood disadvantage are also associated with cognitive decline, however, few studies have integrated this with APOE research. 5 key findings →
Participants: 190 Evidence: low
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We observed that GSK-3β activity was significantly upregulated in ApoE4 mice, accompanied by disruption of the insulin signaling pathway. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In analyses of APOE ε4 carriers, dosage, and genetic risk score, APOE ε4 was associated with lower odds of fluctuating cognition and parkinsonism and higher odds of visual hallucinations. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Employing the random-effects IVW approach, we found that, as indicated by GrimAge, EAA was associated with an increased risk of AD (Odds Ratio [OR] = 1.025, 95% Confidence Interval [CI]: 1.006-1.044, p = 0.009). 5 key findings →
Participants: 63,926 Evidence: low
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Using a 2-sample Mendelian randomization (MR) approach, we evaluated MR evidence for genetically proxied effects of 10 pre-specified gut bacterial classes on type 2 diabetes mellitus (T2DM) and Alzheimer disease (AD), and assessed MR evidence for a direct genetically proxied effect of T2DM on AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
While the β-secretase BACE1 is responsible for the rate-limiting initial step to generate amyloid-β (Aβ) peptides, BACE1 inhibitor clinical trials have been halted due to a lack of efficacy and/or safety concerns at symptomatic/prodromal stages of Alzheimer's disease (AD). 3 key findings →
Evidence: low
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The rising global prevalence of Alzheimer's disease (AD) and mild cognitive impairment (MCI) underscores the urgent need to elucidate their underlying pathogenic mechanisms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings highlight hippocampal atrophy as a key pathway linking Aβ burden to cognitive impairment. 4 key findings →
Evidence: moderate
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Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease without effective treatments. 1 Extracellular amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss are the characteristics of AD neuropathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Missense mutations in the amyloid precursor protein (APP) and presenilin-1 (PSEN1) cause early-onset familial Alzheimer’s disease (FAD) and alter proteolytic production of secreted 38-to-43-residue amyloid β-peptides (Aβ) by the PSEN1-containing γ-secretase complex, ostensibly supporting the amyloid hypothesis of pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We sequenced a total of 38,577 nuclei and detected an average of 2,700 genes per cell. 5 key findings →
Participants: 38,577 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 1,344 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 →