27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Copper and zinc play important roles in Alzheimer disease pathology with recent reports describing potential therapeutics based on modulation of metal bioavailability. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The amino acid sequence of amyloid precursor protein (APP) is highly conserved, and age-related A beta aggregates have been described in a variety of vertebrate animals, with the notable exception of mice and rats. 4 key findings →
Evidence: low
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Obesity has been related to the incidence of dementia but its impact on cognitive performance in persons without dementia is less clear. 4 key findings →
Evidence: moderate
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Cerebrovascular dysfunction contributes to the cognitive decline and dementia in Alzheimer's disease (AD), and may precede cerebral amyloid angiopathy and brain accumulation of the Alzheimer's neurotoxin, amyloid beta-peptide (Abeta). 4 key findings →
Evidence: low
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Our findings confirm and extend previous voxel-based morphometry analyses in ill subjects with schizophrenia. 4 key findings →
Participants: 169 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support evidence of genetic control of brain volume even in adults, particularly of hippocampal and neocortical volume and of cortical volumetric reductions being familial, but do not support measures of subcortical volumes per se as representing intermediate biologic phenotypes. 4 key findings →
Participants: 169 Evidence: low
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The prospective association between adiposity and dementia differs depending on the anthropometric measure used, and is modified by age. 2 key findings →
Participants: 893 Evidence: low
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Mini-Cog screening by office staff is feasible in primary care practice and has measurable effects on physician behavior. 2 key findings →
Participants: 524 Evidence: low
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Alzheimer's disease (AD) is increasing in prevalence. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Competition from another NH-based SCU was associated with the presence of an SCU in a NH [adjusted odds ratio, 3.3; 95% confidence interval (CI), 1.6-6.6] but there were no associations with other measures. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
The epsilon(4) allele of APOE confers a two- to fourfold increased risk for late-onset Alzheimer's disease (LOAD), but LOAD pathology does not all fit neatly around APOE. 3 key findings →
Evidence: low
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Behavioral variant frontotemporal dementia (bvFTD) disrupts our most human social and emotional functions. 2 key findings →
Evidence: low
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High dietary cholesterol and low dietary docosahexaenoic acid (DHA) intake are risk factors for Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Six predefined service goals were set: high acceptability; high appropriate referral rate; successful engagement with people from minority ethnic groups; successful engagement with people with young onset dementia; focus on engagement with mild cases to enable early intervention; and an increase in the overall number of new cases of dementia seen. 3 key findings →
Evidence: moderate
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Deficits of semantic cognition in semantic dementia and in aphasia consequent on CVA (stroke) are qualitatively different. 2 key findings →
Evidence: low
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This study highlights the similarities in the clinical presentation of dementia among the general population and people with DS with a particular emphasis on the earlier appearance of symptoms associated with the frontal lobe dysfunction among adults with DS. 2 key findings →
Participants: 24 Evidence: low
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Chronic inflammation is now considered to be central to the pathogenesis not only of such medical disorders as cardiovascular disease, multiple sclerosis, diabetes and cancer but also of major depression. 2 key findings →
Evidence: low
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The somatodendritic accumulation of hyperphosphorylated tau proteins is an early event preceding the appearance of neurofibrillary tangles (NFT) in Alzheimer's disease (AD) and might be necessary for their formation. 2 key findings →
Evidence: low
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Free radical-mediated oxidative damage is thought to play a role in the pathogenesis of Alzheimer disease. 4 key findings →
Evidence: low
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Alzheimer's disease (AD), the most common neurodegenerative disorder of the elderly, ranks third in health care cost after heart disease and cancer. 2 key findings →
Evidence: low
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The aspartyl protease beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) initiates processing of amyloid precursor protein (APP) into amyloid beta (Abeta) peptide, the major component of Alzheimer disease (AD) plaques. 4 key findings →
Evidence: low
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Neuronal loss occurred in both models, significantly more so in type 2 diabetic BBZDR/Wor rats compared with type 1 diabetic BB/Wor rats and was associated with a ninefold increase of dystrophic neurites. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
SorLA has been recognized as a novel sorting receptor that regulates trafficking and processing of the amyloid precursor protein (APP) and that represents a significant risk factor for sporadic Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
While there is a strong evidence for neural tissue destruction mediated by adaptive autoimmune responses, it is still debated how innate immune responses contribute to neuroinflammatory and neurodegenerative diseases such as multiple sclerosis and Alzheimer's disease. 4 key findings →
Evidence: low
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All solid organs contain resident monocyte-derived cells that appear early in organogenesis and persist throughout life. 4 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 →