28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cerebral amyloid angiopathy (CAA) is currently diagnosed using MRI-based Boston criteria. 4 key findings →
Design: cohort study Participants: 102 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Disease-modifying treatment trials are increasingly advanced to the prodromal or preclinical phase of Alzheimer's disease (AD), and inclusion criteria are based on biomarkers rather than clinical symptoms. 4 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Elevated CSF τ is considered a biomarker of neuronal injury in newly developed Alzheimer's disease (AD) and mild cognitive impairment (MCI) criteria. 4 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is accumulating evidence that synaptic loss precedes neuronal loss and correlates best with impaired memory formation in Alzheimer's disease (AD). 4 key findings →
Participants: 52 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Baseline tau-PET and a composite baseline cognitive score were the strongest independent predictors of cognitive decline. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) neuropathology is extremely heterogeneous, and the evolution from preclinical to mild cognitive impairment until dementia is driven by interacting genetic/biological mechanisms not fully captured by current clinical/research criteria. 2 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The empirical language composite showed superior and consistent sensitivity (faster decline rate) with all three biomarkers. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
= 0.81). NfL levels were not significantly associated with GDS-15 in a population of community-dwelling older adults without dementia. 4 key findings →
Design: cross-sectional Participants: 512 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This cohort study examines the association of serum hyperphosphorylated tau and neurofilament light chain concentrations with psychosis in Alzheimer disease. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This narrative review examines the utility of gait digital biomarkers in Parkinson's disease (PD) research and clinical trials across four contexts: disease susceptibility/risk, disease progression, response to exercise, and fall prediction. 1 key finding →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
, respectively (p-values < 0.05), with p-tau217 demonstrating the highest classification accuracy for Aβ-PET status (AUC = 0.94). 4 key findings →
Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this cohort, 28 participants developed Alzheimer's dementia, 5 frontotemporal dementia, 2 Lewy body dementia, and 2 vascular dementia during the follow-up. 5 key findings →
Participants: 56 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The identification of biomarkers predicting the burden of brain alpha-synuclein (α-syn) pathology in vivo represents a research priority in Lewy body disease (LBD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of 11 subjects with average AUCs above 500,000 units, 7 (64%) developed a central LBD compared to 1 of 20 (5%), with AUCs below the cutoff value (P = 0.0011 by log-rank test). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In PD‐SCD, baseline CSF Aβ42 is associated with cognitive progression. 5 key findings →
Design: cohort study Participants: 50 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 101 FTD patients (64 ± 8 years, 53 men), 230 AD patients (65 ± 10 years, 84 men), and 173 CTR (59 ± 15 years, 67 men) were studied. 5 key findings →
Design: cross-sectional Participants: 101 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The final sample included 1196 cases (505 PD, 26 APD, 476 AD, 189 ALS) and 44,107 control subjects. 5 key findings →
Participants: 1,196 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 0.038) over time. Physical activity was associated with less synaptic dysfunction and cognitive activity with less synaptic dysfunction and lower amyloid burden over time, albeit effect sizes were small. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The 3D-CAM-S severity scores correlated with DRS, delirium duration, and biomarkers of delirium. 1 key finding →
Design: cohort study Participants: 177 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
= 0.025) over 3 years. NfL was not significantly associated with any MRI cSVD marker. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
BIOFACE is a two-year study of clinical, cognition, and biomarkers that will shed light on the physiopathology and the potential utility of plasma and NPEs as non-invasive early diagnostic and prognostic biomarkers in people younger than 65 years. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Axonal degeneration, synaptic dysfunction, astroglial activation, and altered tau metabolism are involved already in preclinical AD. 1 key finding →
Participants: 770 Evidence: low
Full summary, score breakdown and related studies → Original source
We recently demonstrated that the frequencies of biomarker groups defined by the presence or absence of both amyloidosis (A+) and neurodegeneration (N+) changed dramatically by age in cognitively non-impaired subjects. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
We hypothesized that cerebrospinal fluid (CSF) biomarkers of amyloid, neurodegeneration, and endothelial dysfunction would differ between older African Americans and Caucasians with normal cognition and cognitive impairment associated with AD. 3 key findings →
Participants: 135 Evidence: low
Full summary, score breakdown and related studies → Original source
Cardiovascular risk factors, deregulated blood glucose, uric acid metabolism, and inflammation were identified as risk markers for faster disease progression. 2 key findings →
Participants: 135 Evidence: moderate
Full summary, score breakdown and related studies → Original source
10 of the 3,322 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 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 →