Currently there are no effective treatments for many neurodegenerative diseases. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
48/100
CSF Abeta42 was significantly lower and CSF total tau and CSF Ptau-181 significantly higher in EAD patients than FTLD patients and control subjects. 4 key findings →
Evidence: low
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Immunoassays of total tau (t-tau), tau phosphorylated at threonine 181 (p-tau(181)), and beta-amyloid 1-42 (Abeta(42)) concentrations were performed in CSF obtained from participants in the Alzheimer's Disease Neuroimaging Initiative. 4 key findings →
Participants: 195 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The aim of this study was to explore the relationship between cerebrospinal fluid Alzheimer's disease (AD) markers and depression in elderly people. 4 key findings →
Participants: 183 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We selected 57 patients with LBD (dementia with Lewy bodies [DLB], n = 38; Parkinson disease dementia [PDD], n = 19) with available AD CSF biomarkers and neuropsychological data. 4 key findings →
Participants: 38 Evidence: low
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The microRNAs (miRNAs) are potential biomarkers for complex pathologies due to their involvement in the regulation of several pathways. 4 key findings →
Participants: 46 Evidence: low
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We examined 54 volunteers (mean age 70.0 years, 56% women, 51% APOE ɛ4 carriers) with the translocator protein (TSPO) tracer [ 11 C]PBR28 to assess neuroinflammation and with [ 11 C] Pittsburgh compound B (PiB) to assess cerebral Aβ accumulation. [ 11 C]PBR28 and [ 11 C]PiB standardized uptake value ratios (SUVRs) were quantified in 6 regions of interests by using the cerebellar cortex as a pseudo-reference and reference region, respectively. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
48/100
Cognitively normal participants (mean age 57.6 years) from the Gipuzkoa Alzheimer Project study were classified as having high risk (HR; n = 82) or low risk (LR; n = 293) for dementia according to a CAIDE score cutoff of 9. 4 key findings →
Participants: 82 Evidence: low
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48/100
Moreover, we found, in either the whole AD population or both subgroups, a CSF profile in which higher 4 key findings →
Participants: 145 Evidence: low
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Neuropsychological interviews and neuroimaging techniques are traditional diagnostic methods for Alzheimer's disease (AD). 3 key findings →
Participants: 51 Evidence: low
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These results show significant differences in neurogranin and total-tau between typical and atypical patients, which may relate to factors other than disease topography. 4 key findings →
Participants: 27 Evidence: low
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47/100
We hypothesize the population without dementia can be subdivided into participants with and without biological Alzheimer disease (AD) based on the combination of CSF Aβ42 and p-tau/t-tau (represented also by the p-tau/t-tau/Aβ42 ratio). 5 key findings →
Participants: 547 Evidence: low
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MMSE score showed a positive correlation with the Aβ 1-42 concentrations ( r = 0.485; p r = -0.418; p = 0.002). 5 key findings →
Design: cross-sectional Evidence: moderate
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Post-mortem brain tissue from 15 patients dying with a diagnosis of senile dementia of Alzheimer type (SDAT) was compared with tissue obtained from 16 control patients at routine post-mortem. 3 key findings →
Participants: 15 Evidence: low
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In the present study we describe an ELISA to quantify the light subunit of the neurofilament triplet protein (NFL) in CSF. 2 key findings →
Evidence: low
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Increased peripheral and central nervous system cortisol levels have been reported in Alzheimer's disease (AD) and may reflect dysfunction of cerebral components of the hypothalamic-pituitary-adrenal (HPA) axis. 4 key findings →
Evidence: low
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For prediction of dementia in MCI, the AD signature cortical thickness biomarker performed better than hippocampal volume. 3 key findings →
Design: clinical trial Evidence: low
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HIV-associated neurologic disorders (HAND) continue to develop in many patients with HIV. 4 key findings →
Evidence: low
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There is concern that AIDS dementia complex (ADC) may be complicated by Alzheimer disease (AD). 2 key findings →
Evidence: low
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Research progress has provided detailed understanding of the molecular pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Levels of amyloid-β (Aβ) and tau peptides in brain have been associated with Alzheimer disease (AD). 4 key findings →
Participants: 22 Evidence: low
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Alzheimer disease (AD) is a devastating disease and a global health problem, and current treatments are only symptomatic. 4 key findings →
Participants: 242 Evidence: low
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Previous research has shown that elevated blood C-reactive protein (CRP) is associated with increased Alzheimer disease (AD) risk only in APOE ε4 allele carriers; the objective of this study was to examine the interactive effects of plasma CRP and APOE genotype on cognition and AD biomarkers. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) remains a clinical diagnosis but biomarkers from cerebrospinal fluid (CSF) and more lately amyloid imaging with positron emission tomography (PET), are important to support a diagnosis of AD. 4 key findings →
Participants: 64 Evidence: low
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BackgroundAs the prevalence of Alzheimer disease (AD) rises, early identification of at-risk individuals is essential for effective intervention. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
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.
- Role of protein kinase B in Alzheimer's neurofibrillary pathology
- Depressive symptoms and plasma AT(N) biomarkers among cognitively healthy and mild cognitively impaired in a diverse cohort
- CSF Synaptic Biomarkers in the Preclinical Stage of Alzheimer Disease and Their Association With MRI and PET: A Cross-sectional Study
- Cerebrospinal Fluid Biomarkers in Cerebral Amyloid Angiopathy
- Genome-wide meta-analysis for Alzheimer's disease cerebrospinal fluid biomarkers
- Evaluating the reliability of neurocognitive biomarkers of neurodegenerative diseases across countries: A machine learning approach
- CSF Alzheimer Disease Biomarkers: Time-Varying Relationships With MCI Symptom Onset and Associations With Age, Sex, and ApoE4
- Serum levels of S100B and NSE proteins in Alzheimer's disease patients
- Performance of Fully Automated Plasma Assays as Screening Tests for Alzheimer Disease-Related β-Amyloid Status
- Biofluid biomarkers in distinguishing young-onset dementia from primary psychiatric disorders
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →