28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Low levels of cerebrospinal fluid (CSF) beta-amyloid 1-42 (Abeta42) and high total tau (T-tau) are diagnostic for manifest Alzheimer's disease. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
For amyloid positive individuals Aβ42/Aβ40, glial fibrillary acidic protein and p-tau181 were the top predictors of cognitive decline while Aβ42/Aβ40 was prominent for amyloid negative participants across all age groups. 5 key findings →
Design: cross-sectional Participants: 1,185 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
To efficiently implement plasma and cerebrospinal fluid (CSF) biomarkers for staging and prognosis of Alzheimer disease (AD), we must understand their dynamics across disease progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The complexity of neurodegenerative disorders necessitates an integrative approach that incorporates morphological, functional, and molecular biomarkers. 3 key findings →
Participants: 279 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Greater intra-group heterogeneity in ATN abnormality patterns was observed in more severe clinical stages of AD. 5 key findings →
Design: cross-sectional Participants: 665 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Pathophysiologic-constrained ADL provided interpretable, personalized pathologic maps and an AI-derived ADAD score that more closely linked PET pathologic abnormalities with multimodal clinical measures. © RSNA, 2026 3 key findings →
Design: longitudinal study Participants: 7,457 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
P-tau217 demonstrated the most significant inter-group differences, the highest hazard ratio, and best distinguished MCI-Converters from MCI-Nonconverters, with its discriminative performance comparable to that of Aβ-PET measures and multi-plasma biomarker models. 5 key findings →
Design: longitudinal study Participants: 47 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Traumatic brain injury (TBI), a major cause of persistent cognitive impairment (CI), increases the long-term risk of developing dementia, including Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study Participants: 29 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Evidence shows that ADAM10 levels are altered in platelets, plasma, serum, and CSF of individuals with AD. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The results of this proof-of-principle study will be used to assess the potential of target engagement of minocycline for CAA. 1 key finding →
Participants: 60 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
As neuroinflammation is an early event in the pathogenesis of Alzheimer' s disease, new selective antiinflammatory drugs could lead to promising preventive strategies. 3 key findings →
Design: randomized controlled trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Triggering receptor expressed on myeloid cells 2 (TREM-2) is a membrane-bound receptor expressed by microglia and macrophages.
Full summary, score breakdown and related studies → Original source Free full text
Neurogranin (Ng) is a post-synaptic protein that previously has been shown to be a biomarker for synaptic function when measured in cerebrospinal fluid (CSF). 5 key findings →
Participants: 915 Evidence: low
Full summary, score breakdown and related studies → Original source
Aβ misfolding and GFAP showed a strong ability to predict clinical AD risk and may be important early AD risk markers. 1 key finding →
Participants: 68 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These in vivo data support the role of Aβ pathology in the etiology and highlight the potential utility of CSF Aβ42 as an early prognostic biomarker of dementia associated with PD. 3 key findings →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Strong concordance between CSF biomarkers and Aβ-PET status was observed overall, including for cognitively normal participants, further strengthening the association between these markers of AD neuropathological burden for both developmental research studies and for use in clinical trials. 2 key findings →
Participants: 202 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF Aβ42/40 ratio can predict PET amyloid positivity with high accuracy in patients with a range of cognitive disorders when evaluating Aβ pathology independent of tau and neurodegeneration for research purposes. 4 key findings →
Participants: 44 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A panel of structure- and concentration-based plasma amyloid biomarkers may predict conversion to clinical MCI and dementia due to AD in cognitively unimpaired subjects. 3 key findings →
Participants: 203 Evidence: moderate
Full summary, score breakdown and related studies → Original source
GFAP, NfL and pTau 181 levels in plasma were lower in SCD and MCI than in AD patients. 4 key findings →
Participants: 152 Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD), deposition of insoluble amyloid-β (Aβ) is followed by intracellular aggregation of tau in the neocortex and subsequent neuronal cell loss, synaptic loss, brain atrophy, and cognitive impairment. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Two components were identified. Proinflammatory Component 2 was elevated in AD/MCI and in Black/African American participants, and strongly associated with poorer cognition (independently of neurofilament light [NfL], phosphorylated tau 217 [p-tau217], and glial fibrillary acidic protein [GFAP]). 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Analysis of cerebrospinal fluid (CSF) is one of the key tools for the state-of-the-art differential diagnosis of dementias. 3 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source
Discrepancies in diagnostic biomarkers for Alzheimer's Disease (AD) may arise from racial disparities, risk factors, or lifestyle differences. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma and CSF AD biomarkers may perform similarly across diverse populations but future studies in large, diverse cohorts are needed. 3 key findings →
Design: cross-sectional Evidence: low
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 →