Frailty in DS is associated with both ID severity and acquired cognitive decline. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is the leading cause of dementia. 4 key findings →
Participants: 53 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Synaptic loss is the best surrogate for cognitive decline in Alzheimer disease (AD) and is more closely associated with cognitive function than amyloid or tau pathologies. 4 key findings →
Design: cross-sectional Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lecanemab is a humanized monoclonal antibody that binds soluble brain amyloid-β protein, promoting its removal and slowing the underlying process of Alzheimer disease. 1 This mechanism aligns with the amyloid hypothesis, a debated model of Alzheimer disease pathogenesis.1 Only patients with mild cognitive impairment (MCI) or mild dementia due to Alzheimer disease are eligible for lecanemab treatment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
After adjusting for age, sex, race/ethnicity, education, APOE ε4, and physical activity, a greater multimorbidity burden (per 3 additional conditions) was associated with worse overall cognition (standardized β = -0.074, 95%CI -0.104 to -0.043) and biomarkers indicative of greater AD pathology, neurodegeneration, and SVD (Figure 1). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
After a 30-minute educational session, participants showed greater positivity toward an ADRD diagnosis and increased confidence in discussing early detection. 5 key findings →
Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Both taus are very significantly correlated ( p 0,697 in all groups), and with YKL‐40 (r>0.430). 5 key findings →
Participants: 89 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tau protein misfolding and deposition in the brain is a common factor across many neurodegenerative diseases, grouped under the term tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Cognitive impairment associated with Aβ positivity and low tau (A+T‐) is linked to mixed AD. 3 key findings →
Participants: 77 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
After adjusting for age, sex, race/ethnicity, education, APOE ε4, and physical activity, a greater multimorbidity burden (per 3 additional conditions) was associated with worse overall cognition (standardized β =-0.074, 95%CI -0.104 to -0.043) and biomarkers indicative of greater AD pathology, neurodegeneration, and SVD (Figure 1). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In plasma, most complement analytes were not significantly different between spFTD and HC; the exceptions were C4 and FB, significantly decreased in spFTD vs HC ( p = 0.0192 and p = 0.0181, respectively), suggesting complement consumption in classical and alternative pathways. 3 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundRecently published clinical studies suggest that blood-based biomarker tests (BBMTs) for Alzheimer's disease (AD) provide value, but in the U.S., neither public nor private payers currently cover these tests. 1 key finding →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The actual presence of the predicted precursor of Alzheimer's disease amyloid A4 protein, reported by Kang et al. (1987) in the Alzheimer brain, has yet to be verified. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer disease (AD) is a neurodegenerative disorder characterized by extracellular β-amyloid (Aβ) deposition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Prion diseases are characterized by accumulation of misfolded protein, gliosis, synaptic dysfunction, and ultimately neuronal loss. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hemostatic biomarkers were higher in Vascular group compared to Alzheimer group whereas there was no difference in inflammatory biomarkers. 5 key findings →
Participants: 68 Evidence: low
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Dementia is a common feature in Parkinson's disease (PD) and is considered to be the result of limbic and cortical Lewy bodies and/or Alzheimer changes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma amyloid beta protein 1-40 (Abeta40) and Abeta42 levels were quantitated from 28 young Down syndrome (DS) (20-40 years old), 28 age-matched controls, 32 old DS (41-65 years old) and 32 age-matched controls in a sandwich enzyme-linked immunosorbent assay. 1 key finding →
Evidence: low
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Thirty-four years ago, amyloid-β 1-42 peptide was identified in amyloid plaques from brain tissue obtained from patients with Alzheimer disease (AD) and Down syndrome. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The presence of concomitant Alzheimer pathology has been linked to earlier death in cases with dementia with Lewy bodies (DLB). 4 key findings →
Evidence: low
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CSF biomarker studies were performed in 6 patients each with tremor-dominant (TD) and non-tremor-dominant (NT) Parkinson disease (PD) patients, 27 Alzheimer disease (AD) and 17 age-matched controls. 2 key findings →
Evidence: moderate
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Neurosyphilis is a neurological disease that involves infection of the central nervous system with Treponema pallidum. 4 key findings →
Participants: 44 Evidence: low
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Autoimmune encephalitis (AE) is a potentially treatable cause of rapidly progressive dementia that may mimic Creutzfeldt-Jakob disease (CJD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
36/100
Although Alzheimer disease (AD) remains a clinical diagnosis, biomarkers are in use to support the diagnosis. 4 key findings →
Participants: 205 Evidence: low
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Diagnosing Atypical Parkinsonian Syndromes (APS) may be challenging due to overlapping clinical features of Parkinson's disease (PD), and the lack of pathognomonic diagnostic tests. 4 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
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.
- Clinical Relevance of [18F]Florbetaben and [18F]FDG PET/CT Imaging on the Management of Patients with Dementia
- Association of Enlarged Perivascular Spaces With Early Serum and Neuroimaging Biomarkers of Alzheimer Disease Pathology
- Characterization of pre-analytical sample handling effects on a panel of Alzheimer's disease-related blood-based biomarkers: Results from the Standardization of Alzheimer's Blood Biomarkers (SABB) working group
- Cerebrospinal fluid neurofilament light chain protein levels in subtypes of frontotemporal dementia
- Plasma phosphorylated-tau181 as a predictive biomarker for Alzheimer's amyloid, tau and FDG PET status
- Fluid biomarkers for diagnosing dementia: rationale and the Canadian Consensus on Diagnosis and Treatment of Dementia recommendations for Canadian physicians
- Blood biomarkers confirm subjective cognitive decline (SCD) as a distinct molecular and clinical stage within the NIA-AA framework of Alzheimer´s disease
- Recommendations for the diagnosis and management of Alzheimer's disease and other disorders associated with dementia: EFNS guideline
- Neurofilament Light in Serum and Cerebrospinal Fluid of Hip Fracture Patients with Delirium
- 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 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.
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 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 →