27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The presence of an APOE-epsilon4 allele is a determinant of AD risk in whites, but African Americans and Hispanics have an increased frequency of AD regardless of their APOE genotype. 2 key findings →
Design: longitudinal study Participants: 1,079 Evidence: moderate
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The APOE genotype is an important determinant of the risk of dementia. 1 key finding →
Design: cohort study Participants: 134 Evidence: moderate
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Despite methodologic limitations, certain risk factors for delirium seem to be consistent and could help identify high-risk patients. 3 key findings →
Participants: 1,365 Evidence: low
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Delirium is an important independent prognostic determinant of hospital outcomes including new nursing home placement, death or new nursing home placement, and functional decline-even after controlling for age, gender, dementia, illness severity, and functional status. 3 key findings →
Design: cohort study Participants: 727 Evidence: moderate
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To assess age-, sex-, and subtype-specific incidence rates of dementia and to calculate the risk of dementia, the authors performed a large, community-based, prospective cohort study on dementia as part of the Rotterdam Study. 4 key findings →
Design: cohort study Participants: 7,046 Evidence: moderate
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We examined the neuropsychological test performance of a randomly selected community sample of English-speaking non-Hispanic African American and white elders in northern Manhattan. 3 key findings →
Evidence: low
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APOE genotyping does not provide sufficient sensitivity or specificity to be used alone as a diagnostic test for Alzheimer's disease, but when used in combination with clinical criteria, it improves the specificity of the diagnosis. 5 key findings →
Participants: 2,188 Evidence: low
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Recent findings of a linkage between high blood pressure (BP) and later development of dementia have given new prospects on cerebral target-organ damage in hypertension and have added substance to the concept of "preventable senility." 2 key findings →
Design: cohort study Participants: 70 Evidence: moderate
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Lewy bodies and Lewy neurites are the defining neuropathological characteristics of Parkinson's disease and dementia with Lewy bodies. 2 key findings →
Evidence: low
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Familial multiple system tauopathy with presenile dementia (MSTD) is a neurodegenerative disease with an abundant filamentous tau protein pathology. 2 key findings →
Evidence: low
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in 1997, the prevalence of Alzheimer's disease in the United States was 2.32 million (range: 1.09 to 4.58 million); of these individuals, 68% were female. 5 key findings →
Evidence: low
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Abeta1-42 is a self-associating peptide whose neurotoxic derivatives are thought to play a role in Alzheimer's pathogenesis.
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A novel approach to correcting for intensity nonuniformity in magnetic resonance (MR) data is described that achieves high performance without requiring a model of the tissue classes present.
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One of the major symptoms of semantic dementia (or progressive fluent aphasia) is profound word-finding difficulties. 2 key findings →
Design: cross-sectional Evidence: moderate
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The amyloid precursor protein (APP) plays a crucial role in the pathogenesis of Alzheimer's disease.
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Pallido-ponto-nigral degeneration (PPND) is one of the most well characterized familial neurodegenerative disorders linked to chromosome 17q21-22. 5 key findings →
Evidence: low
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Subjects 90 elderly subjects were studied (45 elderly and well persons from the independent living apartments of a continuing care retirement community and 45 patients with probable Alzheimer's disease). 4 key findings →
Participants: 45 Evidence: low
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Two closely related genes, the presenilins ( PS ), located at chromosomes 14q24.3 and 1q42.1, have been identified for autosomal dominant Alzheimer disease (AD) with onset age below 65 years (presenile AD). 4 key findings →
Evidence: low
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Advanced glycation end products (AGEs) have been implicated in the chronic complications of diabetes mellitus and have been reported to play an important role in the pathogenesis of Alzheimer's disease. 1 key finding →
Evidence: low
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The presynaptic protein alpha-synuclein has been implicated in the pathogenesis of Parkinson's disease. 5 key findings →
Evidence: low
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The results confirm that unilateral parkinsonism unresponsive to levodopa and limb ideomotor apraxia are the clinical hallmarks of corticobasal degeneration, and only a minority of patients with corticobasal degeneration present with dementia. 3 key findings →
Evidence: low
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Amyloid deposition is a neuropathological hallmark of Alzheimer's disease. 4 key findings →
Evidence: low
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The G protein Go is highly expressed in neurons and mediates effects of a group of rhodopsin-like receptors that includes the opioid, alpha2-adrenergic, M2 muscarinic, and somatostatin receptors. 4 key findings →
Evidence: low
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Chronic overexpression of the neurite growth-promoting factor S100beta has been implicated in the pathogenesis of neuritic plaques in Alzheimer's disease. 4 key findings →
Evidence: low
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The precursor of the non-Abeta component of Alzheimer's disease amyloid (NACP) (also known as a-synuclein) is a presynaptic terminal molecule that accumulates in the plaques of Alzheimer's disease. 3 key findings →
Evidence: low
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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.
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 →