30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Based on positive/negative results on the different biomarkers, subjects were classified as 'AD-LB-' (n = 304), 'AD+LB-' (n = 335), 'AD+LB+' (n = 158) and 'AD-LB+' (n = 68). 5 key findings →
Design: longitudinal study Participants: 661 Evidence: moderate
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Neurodegenerative diseases (NDs), such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and frontotemporal dementia (FTD), exhibit distinct yet overlapping pathological mechanisms. 2 key findings →
Participants: 10,527 Evidence: low
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While sex differences were not apparent at asymptomatic stages, females showed more rapid declines across all outcomes in symptomatic stages compared to males. 5 key findings →
Design: longitudinal study Participants: 337 Evidence: moderate
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DOPA Decarboxylase (DDC) has been proposed as a cerebrospinal fluid (CSF) biomarker with increased concentrations in Lewy body disorders (LBDs) and highest levels in patients receiving dopaminergic treatment. 2 key findings →
Design: longitudinal study Participants: 71 Evidence: moderate
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Common variants within TMEM106B are associated with risk for frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP). 4 key findings →
Design: cohort study Participants: 518 Evidence: moderate
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Recent studies suggest the existence of brain-first and body-first subtypes within the Lewy body disorder (LBD) spectrum, including Parkinson's disease. 1 key finding →
Participants: 173 Evidence: low
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Thirty-five patients with probable DLB, 37 patients with MCI-LB, and 100 individuals without cognitive impairment were included. 5 key findings →
Design: case-control study Participants: 72 Evidence: moderate
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The LBD-present group had higher QSM values in the SNc (P = 0.008) than the LBD-absent group with no differences in SNr. 5 key findings →
Design: cohort study Participants: 13 Evidence: moderate
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NPS were highly prevalent (≥90%) in early and late bvFTD. 5 key findings →
Design: longitudinal study Participants: 354 Evidence: moderate
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Forty-nine outcomes were presented to survey respondents. 4 key findings →
Design: systematic review Evidence: high
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DTI-ALPS values were significantly lower compared to HC in both DLB (Estimate = -0.084 [-0.14 to -0.03], p = 0.004) and MCI-LB (Estimate = -0.058 [-0.11 to -0.002], p = 0.047) DTI-ALPS was also significantly associated with both baseline (t[147] = 2.22, p = 0.028) and longitudinal decline (t[127] = 2.41,p = 0.017) in cognitive score. 5 key findings →
Design: longitudinal study Participants: 32 Evidence: moderate
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Symptomatic females with genetic FTD had lower frontal cortical thickness than males, and the C9orf72 subgroup showed lower-than-expected frontal cortical thickness for a given level of executive functioning. 5 key findings →
Design: longitudinal study Participants: 394 Evidence: moderate
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We used an untargeted mass spectrometric approach, tandem mass tag proteomics, for the identification of proteomic signatures in genetic frontotemporal dementia (FTD). 5 key findings →
Participants: 238 Evidence: low
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BackgroundWhile cortical atrophy has been widely studied in dementia, emerging evidence highlights the role of subcortical degeneration, particularly in deep gray matter structures such as the thalamus, claustrum, and basal nuclei, in both Alzheimer's disease (AD) and frontotemporal dementia (FTD). 3 key findings →
Design: longitudinal study Participants: 380 Evidence: moderate
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During an average follow-up of 3.63 years, we observed a total of 1 493 individuals developing dementia among 4 341 depressed and 43 214 matched non-depressed individuals (62.4% female; mean [SD] age at baseline 64.4 [11.1] years). 5 key findings →
Design: longitudinal study Participants: 493 Evidence: moderate
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Plasma p‐tau217 has clinical, neuroimaging, and neuropathological correlates in sporadic FTD and may identify FTD cases with AD co‐pathology. 1 key finding →
Design: longitudinal study Participants: 620 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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Lewy body diseases are common neurodegenerative diseases, including Parkinson's disease (PD) and dementia with Lewy bodies, which lead to both motor and non-motor symptoms. 1 key finding →
Evidence: low
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Females with sporadic bvFTD showed worse compulsive behavior (p = 0.026) and language impairments (p = 0.024) compared to females with genetic bvFTD (n = 152). 5 key findings →
Participants: 152 Evidence: low
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= 0.028). AAS perception stratifies FTD syndromes and constitutes a "real-world audiogram" in these diseases. 1 key finding →
Design: case-control study Evidence: moderate
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Nuclear clearance and cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP-43) are observed in many neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 1 key finding →
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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 (3.4% 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 →