Down syndrome (DS) is a major cause of mental retardation and congenital heart disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Down syndrome (DS) is a major cause of mental retardation and congenital heart disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We report the development and validation of an MDS-based cognitive index, the MDS Cognition Scale (MDS-COGS), by evaluating it against two popular dementia rating scales, the Global Deterioration Scale (GDS) and the Mini-Mental State Examination (MMSE). 4 key findings →
Design: cross-sectional Participants: 133 Evidence: low
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Several studies have reported an association of the apolipoprotein E allele epsilon 4 (APOE*4) to familial and sporadic late-onset Alzheimer's disease (LOAD). 4 key findings →
Evidence: low
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These results suggest that management of patients with advanced DAT on a DSCU using a palliative care philosophy may result in less patient discomfort and lower costs than management on a TLTC. 2 key findings →
Design: cohort study Evidence: moderate
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CAG trinucleotide expansion is the molecular basis of Huntington's disease worldwide and is a highly sensitive and specific marker for inheritance of the disease mutation. 4 key findings →
Participants: 1,007 Evidence: low
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Among the 2446 patients who received tacrine in clinical trials, ALT levels greater than the upper limit of normal (ULN) occurred on at least one occasion in 1203 patients (49%), ALT levels greater than three times the ULN occurred in 621 patients (25%), and ALT levels greater than 20 times the ULN occurred in 40 patients (2%). 5 key findings →
Design: open-label trial Participants: 2,446 Evidence: low
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The Cognitive Abilities Screening Instrument (CASI) has a score range of 0 to 100 and provides quantitative assessment on attention, concentration, orientation, short-term memory, long-term memory, language abilities, visual construction, list-generating fluency, abstraction, and judgment.
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Correlational analysis of cerebral metabolic (rCMRglc) data obtained with positron emission tomography (PET) assesses group differences and has demonstrated reduced frontal-parietal rCMRglc interdependencies in Alzheimer's disease (AD). 2 key findings →
Design: longitudinal study Participants: 15 Evidence: moderate
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A cohort of patients was followed up longitudinally and the likelihood of arriving at two cognitive end points was assessed using the Cox proportional hazards model and eight explanatory variables. 4 key findings →
Participants: 135 Evidence: moderate
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Ventricular enlargement and white matter lesions are frequent findings on cerebral magnetic resonance imaging scans of elderly subjects. 4 key findings →
Participants: 90 Evidence: moderate
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A genetic classification of Alzheimer disease(s) (AD) is presented. 4 key findings →
Evidence: low
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We sought to determine whether neuropsychological impairment in schizophrenia is related to current age, age at onset, or duration of illness, and whether the pattern of such impairment can be distinguished from that caused by progressive dementias of Alzheimer's type. 4 key findings →
Participants: 38 Evidence: low
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The apolipoprotein E (apoE) type 4 allele (APOE4) is a susceptibility gene for late-onset familial and sporadic Alzheimer disease. 5 key findings →
Evidence: low
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Data from four studies were used to assess the psychometric properties of the 26 IQCODE items. 5 key findings →
Evidence: low
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We studied the clinical features, pathology, and molecular genetics of a family (Mo) with an autosomal dominant disinhibition, frontal lobe dementia, parkinsonism, and amyotrophy. 5 key findings →
Evidence: low
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The Alzheimer A beta amyloid peptide (A beta) is the principal proteinaceous component of amyloid associated with Alzheimer disease (AD). 4 key findings →
Evidence: low
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These Canadian estimates of the prevalence of dementia fall toward the upper end of the ranges in other studies, whereas the estimates for Alzheimer's disease fall in the middle of the ranges. 2 key findings →
Participants: 9,008 Evidence: low
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The 39- to 43-amino acid amyloid beta-protein (A beta), which is progressively deposited in cerebral plaques and blood vessels in Alzheimer disease (AD), is secreted by cultured human cells during normal metabolism. 4 key findings →
Evidence: low
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An association between the 19q13.2 chromosomal region and Alzheimer's disease (AD) has been reported in AD families and for sporadic AD. 5 key findings →
Participants: 36 Evidence: low
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The neuropsychological tests developed for the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) are currently used to measure cognitive impairments of Alzheimer's disease (AD) in clinical investigations of this disorder.
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Stroke is considered the second most common cause of dementia, but the magnitude of the risk posed by stroke has not been fully clarified. 3 key findings →
Evidence: moderate
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The apoE epsilon 4 allele may be associated with decreased cognitive function in discordant twin pairs. 5 key findings →
Evidence: low
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Nonresponders in community surveys of the elderly appear to be disproportionately cognitively impaired. 3 key findings →
Design: cross-sectional Evidence: low
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We have investigated the possible effect of estrogen on the metabolism of the Alzheimer amyloid precursor protein (APP). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →