28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Several concepts, which in the aggregate get might be used to account for "resilience" against age- and disease-related changes, have been the subject of much research.
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The aim of this study was to compare brain glial fibrillary acidic protein (GFAP) levels to the modifications of cognitive functions (Blessed test score [BTS]), the density of the main neuropathological lesions (senile plaques [SP] and neurofibrillary tangles [NFT]), and the density of the two main subtypes of beta A4 deposits (classic plaques and diffuse deposits) in a series of patients with normal aging and senile dementia of the Alzheimer type of various degrees of severity. 3 key findings →
Evidence: low
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The GFAP mRNA levels were compared to the density of the senile plaques (SP) in postmortem brain samples of 8 cases, either non-demented or affected by senile dementia of the Alzheimer type. 2 key findings →
Evidence: low
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Our observations suggest functional tau disturbance in DS brains during development, rather than axonal loss. 1 key finding →
Evidence: low
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Senile myoclonic epilepsy of Genton is a newer epileptic syndrome of the older patients with Down syndrome associated with an Alzheimer-type dementia. 1 key finding →
Evidence: low
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A descriptive study using a transversal national online survey to evaluate the prevalence and characteristics of behavioral and psychological symptoms (BPSD) of dementia with Lewy bodies (DLB), and specifically, the perpetration of violent acts against primary caregivers. 196 responses, obtained in one month, were analyzed. 5 key findings →
Evidence: low
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We evaluated the allele (and genotype frequencies in 60 Down syndrome (DS), 25 mothers and 57 controls from Sicily and its relation with mental retardation. 2 key findings →
Evidence: low
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SET is a multifunctional protein, but when present in the cytoplasm, acts as a powerful inhibitor of phosphatase 2A. We previously observed that in CA1 of Down syndrome (DS) patients, the level of SET is increased, and SET is translocated to the cytoplasm and associated with the hyperphosphorylation of tau at ser202/thr205. 2 key findings →
Evidence: low
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Type 2 diabetes (T2D) and dementia frequently co-occur, yet the biological mechanisms underlying this comorbidity remain incompletely understood. 1 key finding →
Evidence: low
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Evidence: low
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Cerebral small vessel disease can manifest as vascular dementia, typically associated with vascular risk factors or cerebral amyloid angiopathy, and more rarely associated with hereditary conditions. 5 key findings →
Evidence: low
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In common forms of Alzheimer disease (AD), anterograde memory impairment is the first deficit to occur. 4 key findings →
Evidence: low
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Stroke and dementia are leading causes of death and disability worldwide, requiring enhanced preventive strategies. 1 key finding →
Evidence: low
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• Brain health depends on certain environmental resources of which socioeconomically disadvantaged people in particular are deprived. • Resource deprivation may increase dementia risk due to reduced attainment for deprived populations. • Improving attainment across the lifetime for disadvantaged individuals should be a public health priority for dementia prevention. 1 key finding →
Evidence: low
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Three hundred adult patients were included in the study. 5 key findings →
Evidence: low
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This real-life study aims to describe and compare the characteristics of patients who do or do not receive speech therapy after a memory consultation. 4 key findings →
Evidence: moderate
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The locus of the gene PTK2B encoding the tyrosine kinase Pyk2 has been associated with the risk of late-onset Alzheimer’s disease, the predominant form of dementia. 3 key findings →
Evidence: low
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In human brain extracts, most proteins of pathological interest in Alzheimer's disease are insoluble and their analysis is often performed on denatured and reduced samples by immunoblotting after electrophoresis on polyacrylamide gel in presence of sodium dodecyl sulfate. 3 key findings →
Evidence: low
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Intellectual disability (ID) found in Down syndrome (DS), which is characterized by an extra copy of 234 genes on Chr21 is poorly understood. 4 key findings →
Evidence: low
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Blood biomarkers are increasingly used to support the diagnosis and monitoring of neurodegenerative diseases. 4 key findings →
Design: cross-sectional Participants: 5,123 Evidence: low
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In neurodegenerative diseases, the diagnostic value of α-synuclein seed amplification assay (αSAA) in routine clinical practice and its relationship with cognitive performance and fluid biomarkers remains incompletely characterized. 4 key findings →
Participants: 398 Evidence: moderate
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BackgroundPathogenic variants in GCH1 have been associated with Parkinsons disease (PD), but the clinical phenotype and longitudinal disease course of GCH1-associated PD remain incompletely characterized. 5 key findings →
Design: longitudinal study Participants: 22,825 Evidence: moderate
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Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood. 1 key finding →
Evidence: low
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ObjectiveTo determine whether a multi-trait polygenic profile for dementia is associated with dementia- and disability-free survival in middle-aged and older adults. 5 key findings →
Design: longitudinal study Evidence: moderate
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White matter hyperintensities (WMH), a key MRI-marker of cerebral small vessel disease (cSVD), are common in older adults and associated with an increased risk of stroke and dementia. 5 key findings →
Participants: 46,944 Evidence: moderate
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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. 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.
1,034 records (3.6% 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 →