27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We measured the activities of choline acetyltransferase (ChAT) in the post mortem frontal cortex in 32 Alzheimer's disease (AD) patients with different apolipoprotein E (apoE) genotypes. 4 key findings →
Evidence: low
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The genetics of Alzheimer disease (AD) are complex and not completely understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Phospholipase A2 (PLA2) is a key-enzyme in the metabolism of membrane phospholipids. 4 key findings →
Participants: 23 Evidence: low
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Seven female patients with mild to moderate dementia of the Alzheimer type (DAT) were treated with long-term, low-dose estrogen replacement therapy (ERT) over a period of 5-45 months. 4 key findings →
Evidence: low
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Formalin-fixed postmortem brain tissue from 14 HIV-infected adult patients, with previous repeated neurological and neuroradiological examinations, was studied by immunohistochemical and molecular biological methods. 4 key findings →
Evidence: low
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Among the elderly, the prevalence of Alzheimer's disease and multi-infarct dementia, as opposed to depression, increases steeply with age. 2 key findings →
Design: clinical trial Evidence: low
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Neurodegenerative processes in Alzheimer disease (AD) are thought to be driven in part by the deposition of amyloid beta (A beta), a 39- to 43-amino acid peptide product resulting from an alternative cleavage of amyloid precursor protein. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Based on this study, type and degree of cognitive impairment are better predictors of driving skills than age or medical diagnosis per se. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Evidence that dying occurs as a natural, final event in the wholeness of human life is culturally, artistically, and scientifically persuasive. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The lin-12 and glp-1 genes of Caenorhabditis elegans are members of the lin-12/Notch family of receptors for intercellular signals that specify cell fate. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most common cause of progressive intellectual failure. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The brains of 46 control subjects and 21 Alzheimer's disease (AD) patients were studied to determine whether there are age-related or AD-related changes in the vasoactive intestinal polypeptide (VIP) neuron population of the human suprachiasmatic nucleus (SCN). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down's syndrome (DS) or trisomy 21 is the most common genetic cause of mental retardation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Volga German kindreds are a group of seven related families with autosomal dominant early-onset Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Fas antigen (CD95) is a cell surface protein that mediates apoptosis. 2 key findings →
Evidence: low
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A significant minority of degenerative dementias lack distinctive inclusion bodies, plagues or tangles on pathological examination. 1 key finding →
Evidence: low
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The purpose of this study was to determine cerebral myo-inositol (mI) in adults with Down syndrome (DS), and to trace the chronobiology of DS to Alzheimer disease (AD). 5 key findings →
Evidence: low
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In this clinical study the cerebrospinal fluid (CSF) level of a novel form of the beta-amyloid peptide (A beta) extending to position 42 (A beta 42) was determined in patients with Alzheimer's disease (AD) as well as controls. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta-protein (A beta), the principal constituent of senile plaques seen in Alzheimer's disease (AD), is derived by proteolysis from the beta-amyloid precursor protein (beta PP). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The data from the present study do not lend support to the idea that low affinity, open channel NMDA receptor blockers are also effective in models of epilepsy at doses having little effect on physiological processes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The etiology of neurodegenerative diseases remains enigmatic; however, evidence for defects in energy metabolism, excitotoxicity, and for oxidative damage is increasingly compelling. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As many as 45% to 80% of nursing home residents have pain that contributes materially to functional impairment and decreased quality of life. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The dominantly inherited ataxias comprise a series of clinical phenotypes that include ataxia, dysarthria, dysmetria, and intention tremor resulting from the involvement of the cerebellum and its afferent and efferent pathways. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We reviewed 46 published reports associating cigarette smoking and Parkinson's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Fifty patients with liver cirrhosis underwent neurological, psychometric, electroencephalographic and biochemical examination as well as cranial magnetic resonance imaging (MRI) to study the incidence of pallidal lesions in cirrhotics and their correlation to liver function, as well as to neurological and mental state. 5 key findings →
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 →