Menopause is a major biological transition that may influence women's late-life brain health. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Menopause is a major biological transition that may influence women's late-life brain health. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Both apolipoprotein E (apoE) and 24(S)-hydroxycholesterol are involved in the pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The cholesterol transporter ATP-binding cassette transporter A1 (ABCA1) moves lipids onto apolipoproteins including apolipoprotein E (apoE), which is the major cholesterol carrier in the brain and an established genetic risk factor for late-onset Alzheimer disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Chronic psychological stress is one of the most important triggers and environmental risk factors for neuropsychiatric disorders. 4 key findings →
Evidence: low
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Animal work investigating the consequences of maternal high-fat diet (mHFD) revealed in the offspring a maternal immune activation (MIA) phenotype associated with increased inflammatory signals. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation is a prominent feature of Alzheimer disease (AD) and other chronic neurodegenerative disorders. 4 key findings →
Evidence: low
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Lesions in such chronic neurodegenerative disorders as Alzheimer disease (AD), Parkinson disease, the parkinsonism dementia complex of Guam, and amyotrophic lateral sclerosis have associated with them a variety of proteins known to be involved in inflammatory processes. 4 key findings →
Evidence: low
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Key Points Disasters cause significant human suffering, and patients with kidney diseases are uniquely vulnerable. 4 key findings →
Evidence: low
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Family caregivers provide essential care and support for individuals living with dementia, yet their contributions and needs are often unrecognized within formal health care systems. 1 key finding →
Design: longitudinal study Evidence: moderate
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Involvement of the immune system in the pathogenesis of Alzheimer's disease was demonstrated in two ways: by the attachment of complement proteins to diseased tissue, and by the activation of cells associated with the immune system. 1 key finding →
Evidence: low
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Individuals with Down syndrome (DS) will inevitably develop Alzheimer disease (AD) neuropathology sometime after middle age, which may be attributable to genes triplicated in individuals with DS. 1 key finding →
Evidence: low
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Retinas of transgenic mice harboring a mutant presenilin (PS1) and a mutant APP gene were processed for TUNEL and immunohistochemistry with antibodies against APP, amyloid-beta, monocyte chemotactic protein (MCP)-1, and F4/80. 4 key findings →
Evidence: low
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Transactivation-responsive DNA-binding protein 43 (TDP-43) is a component of pathological inclusions in amyotrophic lateral sclerosis and several forms of sporadic and familial frontotemporal lobar degeneration. 4 key findings →
Evidence: low
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Enriched populations of human microglial cells were isolated from mixed cell cultures prepared from embryonic human telencephalon tissues. 4 key findings →
Evidence: low
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The expression of the purinergic receptor subtype P2X(7)R, a nonselective cationic channel activated by high levels of adenosine triphosphate (ATP), has been studied in adult microglia obtained from Alzheimer disease (AD) and nondemented (ND) brains, in fetal human microglia exposed to Abeta(1-42) peptide and in vivo in Abeta(1-42)-injected rat hippocampus. 4 key findings →
Evidence: low
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Oxidative stress induced by inhibition of glutathione (GSH) biosynthesis with D,L-buthionine-S,R-sulfoximine (BSO) causes human microglia, human astrocytes, THP-1 cells, and U373 cells to secrete materials toxic to human neuroblastoma SH-SY5Y cells and stimulates them to release TNF-alpha, IL-6, and nitrite ions. 4 key findings →
Evidence: low
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Plasma Aβ 42/40 , p‐tau‐181, and NfL differ in those with CAA and together can discriminate CAA from healthy controls. 4 key findings →
Evidence: low
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Dementia is a clinical syndrome of widespread progressive deterioration of cognitive abilities and normal daily functioning. 5 key findings →
Evidence: low
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Neuroinflammation is a central feature of Alzheimer disease (AD). 4 key findings →
Evidence: low
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Localization of beta-2 integrins in normal and Alzheimer disease temporal cortex was studied immunohistochemically. 4 key findings →
Evidence: low
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Cells expressing leucocyte common antigen (LCA) as well as T-cytotoxic-suppressor (T8) and T-helper-inducer (T4) antigens were detected in significant numbers in the hippocampus and temporal cortex of Alzheimer but not normal brain tissue. 4 key findings →
Evidence: low
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Two basic discoveries have spurred research into inflammation as a driving force in the pathology of Alzheimer disease (AD). 4 key findings →
Evidence: low
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Co-existing neuropathology was frequent, even among individuals without clinical dementia. 5 key findings →
Evidence: moderate
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Mild cognitive impairment (MCI) describes a state of cognitive functioning that is below defined norms, yet falls short of dementia in severity. 1 key finding →
Evidence: low
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beta-Amyloid peptide (Abeta) is generated by two cleavages of amyloid precursor protein (APP). 4 key findings →
Evidence: low
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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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →