Changes in CSF biomarker levels may identify early neurodegenerative processes of Alzheimer disease. 2 key findings →
Design: longitudinal study 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.
The global prevalence of dementia is as high as 24 million, and has been predicted to quadruple by the year 2050. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
54/100
Dementia is one of the most common and important aspects of Parkinson's disease and has consequences for patients and caregivers, and has health-related costs. 2 key findings →
Evidence: low
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The diagnosis and treatment of synucleinopathies such as Parkinson disease and dementia with Lewy bodies would be aided by the availability of assays for the pathogenic disease-associated forms of α-synuclein (αSyn D ) that are sufficiently sensitive, specific, and practical for analysis of accessible diagnostic specimens. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results revealed a universal applicability of the "A/T/N" framework in a Chinese population and established an optimal diagnostic model consisting of cost-effective and non-invasive approaches for diagnosing AD. 2 key findings →
Participants: 411 Evidence: moderate
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Our results demonstrate that unsupervised digital memory assessments might be used for diagnosis and prognosis in Alzheimer's disease, potentially in combination with plasma biomarkers. 4 key findings →
Evidence: low
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These findings highlight LBP prevalence in DSAD but suggest current SAA may fail to detect limited αSyn deposition. 4 key findings →
Participants: 270 Evidence: moderate
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) beginning in October 2004, is a 6-year research project that studies changes of cognition, function, brain structure and function, and biomarkers in elderly controls, subjects with mild cognitive impairment, and subjects with Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's Disease (AD) currently affects more than 5 million Americans, with numbers expected to grow dramatically as the population ages. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These plasma ceramides may be early indicators of AD progression. 3 key findings →
Design: cross-sectional Participants: 25 Evidence: low
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The choroid plexus (ChP) is a major source of cerebrospinal fluid (CSF) production, with a direct and indirect role in protein clearance, and pathogenesis of Alzheimer's disease (AD). 3 key findings →
Participants: 509 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Pathological hallmarks of Alzheimer's disease (AD) are deposits of amyloid beta (Aβ) and hyper-phosphorylated tau aggregates in brain plaques. 4 key findings →
Participants: 13 Evidence: low
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Using quantitative polymerase chain reaction techniques, we measured circulating cell-free mitochondrial DNA (mtDNA) in cerebrospinal fluid (CSF) from study participants, selected from a cohort of 282 subjects, who were classified according to their concentrations of amyloid β1-42, total tau, and phosphorylated tau and by the presence or absence of dementia, into asymptomatic subjects at risk of AD, symptomatic patients diagnosed with sporadic AD, presymptomatic subjects carrying pathogenic PSEN1 mutations, and patients diagnosed with frontotemporal lobar degeneration (FTLD). 4 key findings →
Participants: 282 Evidence: moderate
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Alzheimer's disease (AD) neuropathology is associated with neuroinflammation, but there are few useful biomarkers. 4 key findings →
Participants: 100 Evidence: moderate
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We have used these markers and evaluated their performance. 4 key findings →
Participants: 131 Evidence: low
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A total of 401 elderly participants in the Alzheimer's Disease Neuroimaging Initiative who were cognitively normal, who had mild cognitive impairment, or who had AD dementia. 4 key findings →
Participants: 401 Evidence: low
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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
Full summary, score breakdown and related studies → Original source Free full text
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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54/100
We selected 111 patients with probable DLB and CSF available from the Amsterdam Dementia Cohort. 4 key findings →
Participants: 111 Evidence: moderate
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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
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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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Recent studies suggest that plasma phosphorylated tau181 (p-tau181) is a highly specific biomarker for Alzheimer's disease (AD)-related tau pathology. 4 key findings →
Participants: 818 Evidence: low
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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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From across this tag
10 of the 3,069 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.
- Diagnostic performance of plasma p-tau217 in a memory clinic cohort using the Lumipulse automated platform
- Alzheimer disease biomarkers may aid in the prognosis of MCI cases initially reverted to normal
- Blood-based biomarkers across the Alzheimer's disease continuum in older Korean population
- Decoupling Alzheimer Disease Pathologic Abnormalities at PET with Improved Clinical Relevance by Interpretable Adversarial Decomposition Learning
- Performance of Cerebrospinal Fluid Biomarkers of Alzheimer Disease in a Memory Clinic in Norway
- β-Amyloid and tau biomarkers and clinical phenotype in dementia with Lewy bodies
- Constraint Based Metabolic Modeling Identifies Robust Biomarkers and Therapeutic Target Combinations in Alzheimer Disease
- Cerebrospinal fluid alpha-synuclein in neurodegenerative disorders-a marker of synapse loss?
- Soluble amyloid composition links proximal APP processing, fibrillar burden and the p-tau181 response
- Development of language composites for enhanced sensitivity to multiple plasma biomarkers
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 →