The human genome contains over one million short tandem repeats. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The human genome contains over one million short tandem repeats. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TAR DNA binding protein-43 (TDP-43) is the pathologic substrate of neuronal and glial inclusions in frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTDL-U) and in amyotrophic lateral sclerosis (ALS). 1 key finding →
Evidence: low
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It has been well established that neuronal loss within the cholinergic nucleus basalis of Meynert (nbM) correlates with cognitive decline in dementing disorders such as Alzheimer's disease (AD). 2 key findings →
Evidence: low
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The aim of this study was to establish the rate of progression from mild cognitive impairment (MCI) to dementia in patients with Parkinson's disease (PD). 3 key findings →
Participants: 34 Evidence: low
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Baseline data of 423 PD patients and 196 HCs yielded no between-group differences in demographic characteristics. 3 key findings →
Evidence: moderate
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At baseline, worse olfaction (lowest tertile) was associated with more severe NMS, including anxiety and autonomic symptoms. 2 key findings →
Design: cross-sectional Evidence: moderate
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It is important to distinguish FTLD from other neurodegenerative diseases like Alzheimer disease (AD), but this may be difficult clinically because of atypical presentations. 4 key findings →
Participants: 30 Evidence: low
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Antemortem CSF samples were collected from 30 patients with FTLD in a single-center validation cohort, and CSF levels of 5 putative FTLD-TDP biomarkers as well as levels of total Tau (t-Tau) and Tau phosphorylated at threonine 181 (p-Tau181) were measured using independent assays. 4 key findings →
Participants: 30 Evidence: moderate
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Using a cross-sectional design, we examined retinal structure in 38 consecutively enrolled patients with FTD and 44 controls using a standard SD-OCT protocol. 4 key findings →
Design: cross-sectional Participants: 46 Evidence: low
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Frontotemporal dementia (FTD) is a pathologically heterogeneous group of presenile neurodegenerative disorders, with or without the deposition of hyperphosphorylated tau protein in affected brain regions. 4 key findings →
Design: case-control study Participants: 18 Evidence: moderate
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α-Synuclein (αSyn) seed amplification assays (SAAs) accurately detect αSyn pathology in dementia with Lewy bodies (DLB). 4 key findings →
Design: cohort study Evidence: moderate
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Misfolded proteins accumulating in several neurodegenerative diseases (including Alzheimer, Parkinson, and Huntington diseases) can cause aggregation of their native counterparts through a mechanism similar to the infectious prion protein's induction of a pathogenic conformation onto its cellular isoform. 2 key findings →
Evidence: low
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We identified 13 patients with a clinical diagnosis of PD who experienced dementia at least 4 years after parkinsonism onset (mean, 10.5 years) and subsequently underwent postmortem examination. 4 key findings →
Participants: 13 Evidence: low
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Through an international consortium, we have collected 37 tau- and TAR DNA-binding protein 43 (TDP-43)-negative frontotemporal lobar degeneration (FTLD) cases, and present here the first comprehensive analysis of these cases in terms of neuropathology, genetics, demographics and clinical data. 92% (34/37) had fused in sarcoma (FUS) protein pathology, indicating that FTLD-FUS is an important FTLD subtype. 4 key findings →
Evidence: low
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The complexity of neurodegenerative disorders necessitates an integrative approach that incorporates morphological, functional, and molecular biomarkers. 3 key findings →
Participants: 279 Evidence: moderate
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In the Rush dataset, we included 1,277 women and 579 men. 5 key findings →
Participants: 1,277 Evidence: low
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APOE ε4) was associated with a greater severity of each of Braak NFT stage [odds ratio (OR) = 3.07, P = 2.34 × 10-32], Thal amyloid phase (OR = 3.57, P = 3.28 × 10-29) and LBD subtype (OR = 1.78, P = 9.85 × 10-9), with similar findings observed in the independent replication series (Braak NFT stage, OR = 2.30, P = 2.70 × 10-11; Thal amyloid phase, OR = 3.17, P = 6.39 × 10-18; LBD subtype, OR = 2.68, P = 3.85 × 10-10). 5 key findings →
Participants: 980 Evidence: low
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Of 11 327 324 Medicare beneficiaries enrolled in hospice between 2010 and 2020 who met eligibility criteria (mean [SD] age, 85.2 [7.5] years; 781 763 [63.0%] female), there were 958 182 (8.4%) with a primary diagnosis of AD, 232 864 (2.1%) with PD, and 49 340 (0.4%) with DLB. 5 key findings →
Design: cohort study Evidence: moderate
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A total of 798 patients (154 with probable DLB and 644 with AD) were included, and the mean age was 81.4 years (SD 6.33). 5 key findings →
Design: cross-sectional Participants: 798 Evidence: moderate
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Of 293 participants screened, 130 were randomized, and 109 (83.8%) completed the study. 5 key findings →
Participants: 293 Evidence: high
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Parkinson's disease (PD) is a neurodegenerative condition that may affect both motor and cognitive function. 1 key finding →
Design: longitudinal study Participants: 115 Evidence: moderate
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In linear mixed models, vascular endothelial growth factor was significantly associated with incident DWI-positive lesions over 1 year. 5 key findings →
Design: cross-sectional Participants: 181 Evidence: moderate
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In contrast, patients with LB pathology alone, in the absence of AD biomarker positivity, had less overall cognitive impairment but more focal dysexecutive and visuospatial deficits. 5 key findings →
Design: longitudinal study Participants: 85 Evidence: moderate
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Cohort 1 included 446 individuals (mean age (SD) 65.2 years (8.9); 203 women), Cohort 2 included 164 individuals (mean age (SD) 49.9 years (12.6); 88 women). 5 key findings →
Design: longitudinal study Participants: 446 Evidence: moderate
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In SPRINT, the overall interaction between age and SBP on WMHv change was not statistically significant ( P =0.18). 5 key findings →
Design: longitudinal study Participants: 172 Evidence: moderate
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10 of the 2,718 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →