27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Anxiety, apathy and depression are common in subjects with mild cognitive impairment (MCI) and may herald Alzheimer's disease (AD). 4 key findings →
Participants: 268 Evidence: low
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Serine protease inhibitors (serpins), the acute phase reactants and regulators of the proteolytic processing of proteins, have been recognized as potential contributors to the pathogenesis of Alzheimer disease (AD). 4 key findings →
Participants: 258 Evidence: low
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Altered proteome profiles have been reported in both postmortem brain tissues and body fluids of subjects with Alzheimer disease (AD), but their broad relationships with AD pathology, amyloid pathology, and tau-related neurodegeneration have not yet been fully explored. 4 key findings →
Design: cross-sectional Participants: 48 Evidence: low
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CSF biomarkers β-amyloid 1-42 (Aβ 42 ), phosphorylated tau 181 (p-tau 181 ), total tau (t-tau), and neurogranin (Ng) can diagnose Alzheimer disease (AD) in life. 4 key findings →
Participants: 61 Evidence: low
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Fluid and imaging biomarkers of Alzheimer disease (AD) are often used interchangeably, but some biomarkers may reveal earlier stages of disease. 4 key findings →
Participants: 322 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Age-related hearing loss (ARHL) has been considered as a promising modifiable risk factor for cognitive impairment and dementia. 4 key findings →
Design: cross-sectional Evidence: moderate
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In the whole cohort, p ‐tau217, NfL, GFAP and p ‐tau181 were significantly increased over time showing more accelerated increase in Aβ+ than Aβ‐ participants. 4 key findings →
Design: longitudinal study Participants: 718 Evidence: moderate
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Plasma p‐tau 217 offers a cost‐effective AD‐specific alternative to tau‐PET and could potentially be implemented for monitoring cognitive changes in AD trials, while amyloid‐PET lacks utility. 1 key finding →
Design: longitudinal study Participants: 141 Evidence: moderate
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A total of 322 participants with p-tau217, GFAP, and NfL analyses were stratified into the EOAD or FTD group based on their diagnosis. 5 key findings →
Design: cohort study Participants: 245 Evidence: moderate
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Of 1441 plasma proteins surveyed, a 12-protein signature significantly predicted cognitive decline (q-value < .05). 5 key findings →
Participants: 300 Evidence: moderate
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Neuropsychiatric symptoms (NPS), commonly concomitant with Alzheimer's disease (AD), substantially impair the quality of life and accelerate disease progression, yet reliable biomarkers for early identification of individuals at high NPS risk remain elusive. 4 key findings →
Design: longitudinal study Participants: 509 Evidence: moderate
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A total of 158 participants were included, with an average age of 75.2 years (SD 7.65). 60.8% (n=96) of patients had AD, and 39.2% (n=62) had LBD. 4 key findings →
Design: cohort study Participants: 96 Evidence: moderate
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Ultrastructural studies of biopsied cortical tissue from the right frontal lobe of 8 patients with mild to moderate Alzheimer's disease (AD) revealed that the number of synapses in lamina III of Brodmann's area 9 was significantly decreased when compared with the number in age-matched control brains (n = 9; postmortem time, less than 13 hours).
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In this real-world dataset, we identified effects of multimorbidities on plasma biomarkers, especially kidney function. 2 key findings →
Design: cross-sectional Participants: 617 Evidence: moderate
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Plasma GFAP effectively distinguished AD dementia from multiple neurodegenerative diseases, gradually increased across the AD continuum, predicted the individual risk of AD progression, and strongly correlated with AD CSF/neuroimaging biomarkers. 2 key findings →
Participants: 818 Evidence: low
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Higher grey matter volumes/cortical thickness and fluorodeoxyglucose uptake have been consistently found in cognitively unimpaired individuals with abnormal Alzheimer's disease biomarkers compared with those with normal biomarkers. 4 key findings →
Participants: 319 Evidence: moderate
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The HCTS pattern represents a definable subgroup of non-AD pathophysiology (i.e., T - [N] + ) that is associated with cognitive impairment. 2 key findings →
Participants: 684 Evidence: low
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This study suggests that the baseline value of amyloid PET and CSF Aβ 42 measures may be useful for screening participants for AD trials; however, brain hippocampus atrophy and hypometabolism are only useful as repeated longitudinal assessments for tracking cognition and disease progression. 3 key findings →
Design: longitudinal study Participants: 262 Evidence: moderate
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Higher sNfL concentrations were associated with worse performance in cognitive tests at baseline, including CERAD (B = −10.084, SE = 2.999, p < 0.001) and MMSE (B = −3.014, SE = 1.293, p = 0.021). 3 key findings →
Design: cross-sectional Participants: 237 Evidence: moderate
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This approach to the detection of individuals at high risk for preclinical AD-identified in single CN individuals using this quantitative ADsig MRI biomarker-may provide investigators with a population enriched for AD pathobiology and with a relatively high likelihood of imminent cognitive decline consistent with prodromal AD. 3 key findings →
Evidence: low
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Systemic vascular health has significant impact on brain structure and function. 3 key findings →
Participants: 390 Evidence: low
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Low Aβ42 was the strongest predictor of clinical progression in patients with subjective complaints. 3 key findings →
Participants: 127 Evidence: low
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CSF synaptic biomarkers, particularly NPTX2, which regulates synaptic homeostasis, relate to cognition and predict progression in AD beyond Aβ1-42 and Tau. 2 key findings →
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
Full summary, score breakdown and related studies → Original source Free full text
The two primary molecular pathologies in Alzheimer's disease are amyloid-β plaques and tau-immunoreactive neurofibrillary tangles. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 830 studies in this tag, 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →