31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The combinations of hearing and proprioceptive impairment and hearing, vision, and proprioceptive impairment, were positively correlated with cDVR (β = 0.087 and p = 0.036, β = 0.110 and p = 0.018, respectively). 3 key findings →
Design: longitudinal study Participants: 174 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The overall frequency of LATE-NC in Black and White decedents was similar (40.8% vs 45.4%). 5 key findings →
Design: longitudinal study Participants: 76 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The APOE ϵ4 allele is a strong risk factor across the LBD spectrum and occurs at an increased frequency in pDLB relative to PDD. 4 key findings →
Design: case-control study Participants: 244 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Use of naproxen or celecoxib did not improve cognitive function. 2 key findings →
Design: longitudinal study Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
This study's findings suggest that PET imaging with [18F]flortaucipir could be used to identify the density and distribution of AD-type tau pathology and the presence of high levels of AD neuropathological change, supporting a neuropathological diagnosis of AD. 4 key findings →
Participants: 64 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Across the whole-sample, the single-modality models indicated significant correlations between the rate of cognitive decline and the first component of each imaging modality. 4 key findings →
Design: longitudinal study Participants: 12 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We have carried out a systematic review of the case files of 242 donors with pathologically verified Parkinson's disease at the Queen Square Brain Bank for Neurological Disorders in an attempt to corroborate the data-driven subtype classification proposed by Lewis and colleagues (Heterogeneity of Parkinson's disease in the early clinical stages using a data driven approach. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Whether mild cognitive impairment (MCI) has a distinct neuropathological profile that reflects an intermediate state between no cognitive impairment and dementia is not clear. 5 key findings →
Design: systematic review Participants: 162 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is the leading cause of dementia worldwide, but the cellular pathways that underlie its pathological progression across brain regions remain poorly understood 1-3 . 4 key findings →
Participants: 48 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Many coronavirus disease 2019 (COVID-19) positive individuals exhibit abnormal electroencephalographic (EEG) activity reflecting "brain fog" and mild cognitive impairments even months after the acute phase of infection. 5 key findings →
Design: systematic review Participants: 19 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We aimed to investigate whether hippocampal TDP-43 is associated with increased rates of hippocampal atrophy. 4 key findings →
Design: longitudinal study Participants: 205 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Aβ-PET was abnormal in 81 participants from J-TRC and 71 participants from BioFINDER. 2 key findings →
Design: cross-sectional Participants: 474 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The primary constituents of plaques (Aβ42/Aβ40) and neurofibrillary tangles (tau and phosphorylated forms of tau [ptau]) are the current leading diagnostic and prognostic cerebrospinal fluid (CSF) biomarkers for AD. 3 key findings →
Design: case-control study Participants: 5,161 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Based on 19 studies the weighted RR for occupational exposure to EMFs was 1.26 (95% confidence interval (CI) 1.07⁻1.50) for ALS, 1.33 (95% CI 1.07⁻1.64) for Alzheimer's disease and 1.02 (95% CI 0.83⁻1.26) for Parkinson's disease. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
This population-based cohort study demonstrates significant association between IBD and subsequent development of dementia. 5 key findings →
Design: cohort study Participants: 1,742 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The mitochondrial cascade hypothesis of Alzheimer's disease (AD) has been portrayed through molecular, cellular, and animal studies; however large epidemiological studies are lacking. 3 key findings →
Design: cohort study Participants: 790 Evidence: moderate
Full summary, score breakdown and related studies → Original source
FBXL7, encodes a subcellular protein involved in phosphorylation-dependent ubiquitination processes and displays proapoptotic activity. 5 key findings →
Design: case-control study Participants: 5,300 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our data highlight the complex interplay between disease, age and cell-type-specific methylation changes in AD risk genes thus offering new perspectives for the validation and interpretation of large EWAS results. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Voxel-wise 18F-MK-6240 analyses revealed that with each decade of A+, the spatial extent of measurable tau spread (i.e. progressed) from regions associated with early to late NFT tau stages. 5 key findings →
Design: cohort study Participants: 537 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuroinflammation is believed to be a key process in Alzheimer's disease (AD) pathogenesis. 5 key findings →
Design: longitudinal study Participants: 1,544 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although AD cases with a CLix score less than 10 had higher cortical tangle count, we found lower percentage of CD68-activated microglia/macrophage burden (median [IQR], 0.46% [0.32%-0.75%]) compared with cases with a CLix score of 10 to 30 (median [IQR], 0.75% [0.51%-0.98%]) and on par with a CLix score of 30 or greater (median [IQR], 0.40% [0.32%-0.57%]; P = .02). 3 key findings →
Design: cross-sectional Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Transgenic models of familial Alzheimer's disease (AD) serve as valuable tools for probing the molecular mechanisms associated with amyloid-beta (Aβ)-induced pathology. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Folic acid is beneficial in patients with AD. 2 key findings →
Participants: 121 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings add to growing evidence that women have a differential tau response to Aβ that may emerge at the point of p-tau secretion. 5 key findings →
Design: cohort Participants: 1,292 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer's disease (AD), amyloid-β (Aβ) triggers the aggregation and spreading of tau pathology, which drives neurodegeneration and cognitive decline. 3 key findings →
Design: cohort Participants: 609 Evidence: moderate
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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,045 records (3.3% of the library) are not peer-reviewed — 966 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events
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