27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
It has remained a matter of debate until now whether amyloid and tangle pathology may be regarded as the main causes of the dementia in Alzheimer's disease (AD) or only as markers of the disease. 3 key findings →
Evidence: low
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Down syndrome remains one of the most common causes of mental retardation. 1 key finding →
Evidence: low
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The senile plaques found within the cerebral cortex and hippocampus of the Alzheimer disease brain contain beta-amyloid peptide (A beta) fibrils that are associated with a variety of macromolecular species, including dermatan sulfate proteoglycan and heparan sulfate proteoglycan. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Spouse-caregivers of Alzheimer's disease patients were randomly assigned to either a treatment group (individual and family counseling, support group participation, and ad hoc consultation) or a control group (only routine support). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The association cortex of Down's syndrome (DS) predictably and prematurely undergoes neurofibrillary degeneration of Alzheimer type. 3 key findings →
Evidence: low
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A major component of amyloid deposits found in Alzheimer disease and Down syndrome is the beta/A4 peptide, which is derived from the Alzheimer amyloid protein precursor (APP). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Frequencies of chromatid aberrations in response to G2-phase x-irradiation were compared in PHA-stimulated blood lymphocytes from healthy control subjects, Down syndrome (DS) patients, and Alzheimer disease (AD) patients. 4 key findings →
Evidence: low
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It has been suggested that microglia, a type of glial cells in the central nervous system, play various important roles in normal and pathologic brains. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Professional and family members of demented individuals, especially if they have experience in terminal care decisions, strongly favor palliative care for end-stage dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The hippocampus plays an essential role in spatial learning. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The major protein subunit of the paired helical filaments (PHF) of Alzheimer disease (AD) is the microtubule-associated protein tau. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glial fibrillary acidic protein (GFAP) mRNA was examined by RNA blot hybridization in three age groups of two cohorts of male F-344 rats and in 47 human postmortem brain samples. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The origin of ramified microglia has been a longstanding controversial issue, with 4 major schools of thought, which state that they are derived (1) from invasion of mesodermal pial elements, (2) from neuroectodermal matrix cells together with the macroglia, (3) from pericytes, and (4) from invasion of monocytes in early development. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The beta-amyloid precursor protein (beta APP) is a membrane-spanning glycoprotein that is the source of the beta-amyloid peptide (beta AP) which accumulates as senile plaques in the brains of patients with Alzheimer's disease. beta APP is normally processed such that a cleavage occurs within the beta AP, liberating secreted forms of beta APP (APPss) from the cell. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The major constituent of the paired helical filaments (PHFs) of Alzheimer's disease is the abnormally phosphorylated form of the microtubule-associated protein, tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We re-examined the relationship among synaptic pathology, subcellular abnormalities within neurites in the plaques and beta-amyloid deposits of Alzheimer's disease (AD) using laser confocal imaging and computer-aided serial section reconstruction techniques. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Reactive oxygen metabolites (ROM), namely superoxide and hydroxyl free radicals and hydrogen peroxide, are produced as a consequence of the physiological metabolic reactions and functioning of the central nervous system. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The progressive neurodegeneration of Alzheimer's disease has been hypothesized to be mediated, at least in part, by beta-amyloid protein. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Reinvestigation of the chemical structure of beta-amyloid peptide (A beta) deposits in the vascular tissue of Alzheimer disease brains revealed that the 42-residue form A beta-(1-42), rather than the more soluble A beta-(1-40) form, is the predominant peptide. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A neuropathological hallmark of Alzheimer disease (AD) is a widespread amyloid deposition. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study examines total formal and informal care costs attributable to Alzheimer's disease for persons living in the community and in institutions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A simple, completely objective scoring system for a clock completion test has been developed which involves only the number of digits placed in the fourth quadrant of a pre-drawn circle. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent findings link altered processing of beta-amyloid precursor protein (beta APP) to disruption of neuronal Ca2+ homeostasis and an excitotoxic mechanism of cell death in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A beta, a nearly insoluble peptide, is generally assumed to irreversibly deposit and accumulate as senile plaques (SP) during the course of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
IgG subclasses were measured in sera from 33 persons with Down syndrome (DS) (mean age 55 +/- 7 years) and 33 age- and sex-matched control individuals using a mouse monoclonal antibody based sandwich enzyme linked immunosorbent assay. 3 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 27,380 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 →