27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
When people are asked to imagine themselves incompetent with a poor prognosis, they decide against life-sustaining treatments about 70 percent of the time. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The secondary structures in solution of the synthetic, naturally occurring, amyloid beta peptides, residues 1 to 42 [beta (1-42)] and beta (1-39), and related fragments, beta (1-28) and beta (29-42), have been studied by circular dichroism and two-dimensional nuclear magnetic resonance spectroscopy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We reanalyzed and compared current prevalence estimates of Alzheimer's disease in Europe. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Quinolinic acid is an "excitotoxic" metabolite and an agonist of N-methyl-D-aspartate receptors. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In patients with Alzheimer's disease (AD), compared with age-matched and young healthy control subjects, visual deficits in the following functions were observed: color, stereoacuity, contrast sensitivity, and backward masking (homogeneous and pattern). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Substituted judgment has been proposed as a method of promoting the autonomy of the mentally incapacitated patient, but little is known about the accuracy of surrogate decision makers in reflecting the true wishes of patients. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The brains of patients with Alzheimer's disease (AD) invariably exhibit neuropathology in the hippocampus and entorhinal cortex when examined postmortem. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Multiple sclerosis (MS) brain tissue, spleen, and PBMC were studied using immunocytochemistry and FACS for immunoreactivity for lymphotoxin (LT) and TNF. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid precursor protein (APP) is thought to be processed aberrantly to yield the major constituent of the amyloid plaques observed in the brains of patients with Alzheimer disease and Down syndrome. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
The amyloid precursor protein (APP) gene codes for the precursor to the beta-protein found in the amyloid deposits of Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Transcriptional regulation of the gene encoding the amyloid precursor protein (APP) may play an important role in the formation of the amyloid depositions observed in Alzheimer disease and Down syndrome patients. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
It was suggested that increased Cu-Zn superoxide dismutase (SOD-1) might be involved in the various biological abnormalities found in Down's syndrome (DS) such as premature aging and Alzheimer-type neurological lesions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The dementia of Alzheimer disease (AD) correlates with the deposition of extracellular amyloid, and this amyloid arises from the abnormal processing of a high molecular weight amyloid peptide precursor (APP), which is a normal cellular protein that is found in both brain and in peripheral tissues in humans. 1 key finding →
Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Neuropathologic and neuroradiologic studies have reported hippocampal abnormalities in schizophrenics. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The structure and function of the chemicals contributing to the three main peaks seen with 1H NMR spectroscopy, N-acetyl-L-aspartate (NAA), creatine/phosphocreatine (Cr), and choline-containing compounds (Cho) is reviewed and the changes seen with these compounds in various disease states are briefly outlined. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies indicated that the formation of a major constituent of Alzheimer's disease (AD) senile plaques, called beta A4-peptide, does not result from normal processing of its precursor, amyloid precursor protein (APP). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We developed a new immunohistochemical method by which normal tau antigenicity can be visualized in paraffin sections of formalin-fixed brain tissue. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To investigate the extent to which whole tau proteins, structurally abnormal tau and fragments of tau are incorporated into neurofibrillary tangles in Alzheimer's disease, an immunocytochemical mapping study using a panel of antibodies to several synthetic human tau peptides has been performed. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The tau-immunoreactive A68 polypeptides found in brains from patients with Alzheimer's disease have been studied by Western blotting using (1) antibodies to synthetic peptides corresponding to sequences that span the complete human tau molecule, and (2) antibodies specific for inserts 1 and 2 found towards the N-terminus of some tau isoforms. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofibrillary tangles (NFTs), a hallmark of Alzheimer disease, are commonly located in perikarya of neurons. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A central unresolved issue in Alzheimer's disease is the origin of the extracellular amyloid beta protein (A beta P) found in senile plaques and its relationship to the dystrophic neurites that intimately surround it. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing attention is being paid to inappropriate medication use in nursing homes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The present study was designed to determine which of the memory tasks included in the CERAD (Consortium to Establish a Registry for Alzheimer's Disease) neuropsychological battery best differentiate patients with early Alzheimer's disease from cognitively normal elderly control subjects and also best distinguish between the various levels of severity of the dementia process. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglial cells and astrocytes are closely associated with nearly all compact deposits of the amyloid beta-protein found in the senile plaques characteristic of Alzheimer's disease and trisomy 21. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →