28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Regeneration of injured nerves is likely occurring in the peripheral nervous system, but not in the central nervous system. 4 key findings →
Design: meta-analysis Evidence: high
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Mild cognitive impairment (MCI), an intermediate state between normal aging and dementia, is characterized by acquired cognitive deficits, without significant decline in functional activities of daily living. 2 key findings →
Evidence: low
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Myeloperoxidase, a heme protein expressed by professional phagocytic cells, generates an array of oxidants which are proposed to contribute to tissue damage during inflammation. 4 key findings →
Evidence: low
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Clinical trials of anti-amyloid-β (Aβ) monoclonal antibodies in Alzheimer disease (AD) infer target engagement from Aβ positron emission tomography (PET) and/or fluid biomarkers such as cerebrospinal fluid (CSF) Aβ42/40. 2 key findings →
Evidence: moderate
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They also suggest that FW elevation occurs in the locus coeruleus to transentorhinal cortex tract, nucleus basalis of Meynert, and hippocampus in the transition from CN to EMCI, while other basal forebrain regions and the entorhinal cortex are not affected until a later stage of AD. 2 key findings →
Evidence: low
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In an aging population with increasing incidence of dementia and cognitive impairment, strategies are needed to slow age-related decline and reduce disease-related cognitive impairment in older adults. 1 key finding →
Evidence: low
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To determine the prevalence of cognitive impairment and dementia in a multi-ethnic community, we examined a population sample of 2,759 elderly (65 years of age and older) African American, Hispanic-Cuban and white non-Hispanic men and women of Dade County, Florida. 1 key finding →
Evidence: low
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In light of recent reports of diminished platelet serotonin concentration and increased plasma serotonin levels in patients with Alzheimer disease (AD), we hypothesized that a state of heightened platelet activation might be present in AD. 4 key findings →
Participants: 91 Evidence: low
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Neurofibrillary degeneration in the nucleus basalis and a loss of its cortical cholinergic projections are prominent components of the neuropathology in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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All concurrent validity correlations followed the expected directionality, with 19/21 inter-scale correlations in the total sample reaching statistical significance (p<0.05), and 17/21 reaching at least a low correlation (0.3). 4 key findings →
Participants: 100 Evidence: low
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SIs on the LASSI-L related to PSI and frPSI uniquely differentiated Amy+ and Amy- participants with aMCI and likely reflect deficits with inhibition and source memory in preclinical AD not captured by traditional cognitive measures. 2 key findings →
Evidence: low
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APOE alleles ε2, ε3, and ε4 account for essentially all the inherited risk of AD associated with this region. 3 key findings →
Evidence: low
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Despite accumulating amyloid burden, cholinergic enzyme activity is stable in the precuneus during prodromal AD. 4 key findings →
Evidence: low
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From a clinical perspective, these data further support the rationale for physicians to provide effective management of CVD risk factors and for patients to be compliant with such recommendations to possibly prevent cognitive decline/dementia. 4 key findings →
Design: open-label trial Evidence: high
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Neurofibrillary tangles (NFT) and β-amyloid plaques are the neurological hallmarks of both Alzheimer's disease and an unusual paralytic illness suffered by Chamorro villagers on the Pacific island of Guam. 3 key findings →
Evidence: low
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These results suggest that mechanisms leading to atherosclerosis might also lead to an increased number of perivascular spaces. 5 key findings →
Participants: 706 Evidence: low
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Tau is a microtubule-associated protein that forms neurofibrillary tangles (NFTs) in the selective vulnerable long projection neurons of the cholinergic basal forebrain (CBF) in Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Cognitive impairment is common in Parkinson's disease (PD). 4 key findings →
Evidence: low
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Participants identified as non-Hispanic White (50%), non-Hispanic Black (30%), or Hispanic (13%). 5 key findings →
Design: cross-sectional Participants: 192 Evidence: low
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The Alzheimer's Disease Sequencing Project (ADSP) undertook whole exome sequencing in 5,740 late-onset Alzheimer disease (AD) cases and 5,096 cognitively normal controls primarily of European ancestry (EA), among whom 218 cases and 177 controls were Caribbean Hispanic (CH). 2 key findings →
Evidence: low
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We aimed to identify new candidate genes potentially involved in early-onset Alzheimer's disease (EOAD). 4 key findings →
Evidence: low
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Regardless of method or adjustment, the resulting heritability estimates were highly variable across populations. 5 key findings →
Participants: 7,024 Evidence: moderate
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Ten‐year Black‐White disparities in prison population are associated with cognitive decline among people racialized as Black starting one year later. 5 key findings →
Participants: 2,300 Evidence: low
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Late-onset Alzheimer disease (LOAD), the most common form of dementia among older adults, is a neurodegenerative disease characterized by brain amyloid-β (Aβ) plaque deposition and neurofibrillary tangles. 4 key findings →
Design: longitudinal study Evidence: moderate
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Participants racialized as Black who lived in places with higher levels of area‐level structural socioeconomic racism experienced lower levels of cognition at baseline and at varying time points in the six‐year period—compared to those in places with lower structural socioeconomic racism. 2 key findings →
Participants: 1,172 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. 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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 →