28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
There is a clear need to develop biomarkers for Parkinson disease (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring disease progression. 4 key findings →
Design: cross-sectional Evidence: moderate
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Compare cognitive and hippocampal volume trajectories in asymptomatic middle-aged and older adults with positive CSF markers of β-amyloid (Aβ) or tau to adults without an Alzheimer disease (AD)-associated biomarker profile. 4 key findings →
Design: cohort study Participants: 78 Evidence: moderate
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There are limited data regarding cerebrospinal fluid (CSF) and plasma biomarkers among patients with Cerebral Amyloid Angiopathy (CAA). 4 key findings →
Design: systematic review Evidence: high
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The aim of this study was to evaluate longitudinal associations of multimodal core 1 AD biomarkers with cognition in a cognitively unimpaired (CU) population at increased risk of AD dementia. 4 key findings →
Design: longitudinal study Participants: 350 Evidence: moderate
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Cerebrospinal fluid (CSF) levels of Abeta peptide 1-42 (Abeta 42), tau, and phosphorylated tau (ptau) are potential biomarkers of Alzheimer disease. 4 key findings →
Design: longitudinal study Participants: 49 Evidence: moderate
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Assessment of Alzheimer's disease (AD)-related neurofibrillary pathology requires a procedure that permits a sufficient differentiation between initial, intermediate, and late stages. 4 key findings →
Evidence: low
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Cerebrospinal fluid (CSF) biomarkers are useful in the diagnosis and the prediction of progression of several neurodegenerative diseases. 2 key findings →
Participants: 535 Evidence: moderate
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Performance was assessed in comparison to clinical diagnosis (blinded to plasma results) and amyloid status (CSF/PET). 4 key findings →
Participants: 268 Evidence: moderate
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AD was common in both AD-related syndromes (110/125 [88%]) and FTLD-related syndromes (45/198 [23%]). 2 key findings →
Participants: 125 Evidence: low
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The pTau217/Aβ42 ratio demonstrated the highest diagnostic accuracy, with an AUC of 0.927 (0.900-0.954). 3 key findings →
Participants: 423 Evidence: moderate
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These findings suggest an association of sHHV infection with white matter volume loss, attentional decline, and astrogliosis. 5 key findings →
Design: cross-sectional Participants: 119 Evidence: moderate
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CSF Aβ 42 and PiB PET showed maximal correlation when collected within 6 years of each other ( R ≈ -0.5). 1 key finding →
Design: longitudinal study Participants: 371 Evidence: moderate
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Higher baseline p-tau181 and NfL were associated with significantly faster decline in most cognitive, physical, and functional outcomes (+1 SD p-tau181: β MMSE = -0.055, 95% CI -0.067 to -0.043, β FCSRT = -0.034, 95% CI -0.043 to -0.025, β fluency = -0.029, 95% CI -0.038 to -0.020, β SPPB = -0.040, 95% CI -0.057 to -0.022, and β 4IADL = -0.115, 95% CI 0.091-0.140. +1 SD NfL: β MMSE = -0.039, 95% CI -0.053 to -0.025, β FCSRT = -0.022, 95% CI -0.032 to -0.012, β fluency = -0.014, 95% CI -0.024 to -0.004, and β 4IADL = 0.077, 95% CI 0.048-0.105). 4 key findings →
Participants: 1,938 Evidence: moderate
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These findings suggest that promoting CVH in older adults may help alleviate the burden of neurodegenerative diseases, particularly among Black adults, who are known to experience a higher prevalence of cardiovascular disease. 5 key findings →
Design: cohort study Participants: 1,018 Evidence: moderate
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Delirium following surgery is common and associated with adverse outcomes. 2 key findings →
Design: cohort study Participants: 282 Evidence: moderate
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During follow-up, 57 (42%) patients with MCI developed Alzheimer's disease, 21 (15%) developed other forms of dementia, and 56 (41%) remained cognitively stable for 5.2 years (range 4.0-6.8). 1 key finding →
Evidence: low
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CVR was significantly associated with cognitive performance independently of AD pathology. 5 key findings →
Design: cross-sectional Participants: 28 Evidence: low
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This article gives a comprehensive overview of cytokine and other inflammation associated protein levels in plasma, serum and cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD) and mild cognitive impairment (MCI). 2 key findings →
Design: longitudinal study Evidence: moderate
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Baseline CSF was collected from 512 patients with Alzheimer disease (AD) and 272 patients with other types of dementia (OD), 135 patients with a psychiatric disorder (PSY), and 275 patients with subjective memory complaints (SMC). 4 key findings →
Participants: 512 Evidence: moderate
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Although advancing age is the strongest risk factor for the development of symptomatic Alzheimer disease (AD), recent studies have shown that there are individual differences in susceptibility to age-related alterations in the biomarkers of AD pathophysiology. 4 key findings →
Design: cross-sectional Participants: 268 Evidence: moderate
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Measures of neuronal loss are likely good surrogates for clinical and radiological disease progression in Alzheimer disease (AD). 4 key findings →
Design: longitudinal study Participants: 23 Evidence: moderate
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In this retrospective study, GAP-43 was measured in participants from the AD Neuroimaging Initiative (ADNI) cohort using an in-house ELISA method, and levels were compared between groups, both cross-sectionally and longitudinally. 4 key findings →
Participants: 786 Evidence: moderate
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A growing body of evidence suggests that the plasma concentration of the neurofilament light chain (NfL) might be considered a plasma biomarker for the screening of neurodegeneration in Alzheimer's disease (AD). 4 key findings →
Participants: 25 Evidence: low
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The relative performance of semi-quantitative amyloid positron emission tomography (PET) and cerebrospinal fluid (CSF) markers in diagnosing Alzheimer's disease (AD) and predicting the cognitive evolution of patients with mild cognitive impairment (MCI) is still debated. 4 key findings →
Design: cross-sectional Participants: 677 Evidence: moderate
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To test whether cerebrospinal fluid (CSF) growth-associated protein 43 (GAP-43) concentration is elevated in Alzheimer's disease (AD) dementia and its associations with other hallmarks of AD, we examined the CSF GAP-43 measurements of 787 participants (245 cognitively normal (CN), 415 individuals with mild cognitive impairment (MCI) and 127 individuals with AD dementia) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study. 4 key findings →
Design: longitudinal study Participants: 787 Evidence: moderate
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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.
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →