38/100
Alzheimer's disease (AD) displays a long asymptomatic stage before dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
As we age, we experience changes in our nighttime sleep and daytime wakefulness. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The nature of fluid dynamics within the brain parenchyma is a focus of intensive research. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recent failures of potential disease-modifying drugs for Alzheimer's disease (AD) may reflect the fact that the enrolled participants in clinical trials are already too advanced to derive a clinical benefit. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The purpose of this study was to explore how liraglutide affects AD-like pathology and cognitive function in APP/PS1/Tau triple transgenic (3 × Tg) Alzheimer disease (AD) model mice. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Millions of children and young adults are exposed to fine particulate matter (PM2.5) and ozone, associated with Alzheimer's disease (AD) risk. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
S100B is a Ca 2+ -binding protein mainly concentrated in astrocytes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recent paradigm shift towards a more biologically oriented definition of Alzheimer's disease (AD) in clinical settings increases the need for sensitive biomarkers that can be applied in population-based settings. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies (DLB) is a common subtype of dementia in the elderly. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The reliability of cerebrospinal fluid (CSF)-tau and CSF-beta-amyloid assays for diagnosis of Alzheimer's disease and other dementing disorders such as frontotemporal dementia (FTD), dementia with Lewy bodies (DLB) and Creutzfeldt-Jakob disease (CJD) is reviewed. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
In the PD group, 13 had normal cognition, 4 had subjective and 14 mild cognitive impairment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
It is a challenge to differentiate between HIV-associated neurocognitive disorders (HAND) and other types of neurocognitive disease in the ageing HIV-infected population. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of misfolded α-synuclein (α-syn) protein in Lewy bodies and neurites is the cardinal pathologic feature of Parkinson disease (PD), but abnormal deposition of other proteins may also play a role. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this study we aimed to evaluate the possibility of using cerebrospinal fluid (CSF) tau, Abeta(1-42) and inflammatory cytokines for diagnosis of Alzheimer's disease (AD) and vascular dementia (VD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies have associated clusterin (CLU) variants with Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the presence in the brain of amyloid plaques, consisting predominately of the amyloid β peptide (Aβ), and neurofibrillary tangles, consisting primarily of tau. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A growing body of evidence supports the application of the neurochemical dementia diagnostics (NDD) biomarkers for the diagnosis of dementing conditions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sphingolipids are important in many brain functions but their role in Alzheimer's disease (AD) is not completely defined. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Matrix metalloproteinases (MMPs) are a family of enzymes able to degrade components of the extracellular matrix, which is important for normal blood-brain barrier function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increased cerebrospinal fluid (CSF) tau protein levels are generally considered to provide a sensitive marker of neurodegenerative processes such as Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta protein 40 (Abeta40) and 42 Abeta42, major components of senile plaque amyloids, are physiological peptides present in the brain, cerebrospinal fluid (CSF) and plasma. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
As dementia is a fast-growing health care problem, it is becoming an increasingly urgent need to provide an early diagnosis in order to offer patients the best medical treatment and care. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A significant proportion of patients with dementia with Lewy bodies (DLB) show Alzheimer's disease (AD) pathology like senile plaques and neurofibrillary tangles. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
38/100
Tau is the main protein of paired helical filaments. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) has become a matrix for biomarker discovery and development in recent years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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.
- Diagnostic accuracy of automated Lumipulse plasma pTau-217 in Alzheimer's disease: a real-world study
- Neurofilaments and tau proteins in cerebrospinal fluid and serum in dementias and neuroinflammation
- False positive plasma p-tau217 results associated with heterophilic antibody interference: A potential clinical pitfall
- Clinical utility of plasma p-tau217 in identifying abnormal brain amyloid burden in an Asian cohort with high prevalence of concomitant cerebrovascular disease
- Alzheimer's Disease polygenic risk, the plasma proteome, and dementia incidence among UK older adults
- CSF Aβ40 and P-Tau181 Might Differentiate Atypical from Typical AD Phenotypes: Preliminary Evidence
- Quantitative Systems Pharmacology Analysis of Amyloid Aggregation and Hippocampal Atrophy Trajectories in Alzheimer’s Disease by APOE4 Genotype and Valiltramiprosate/ALZ-801 Treatment
- A cross-sectional study of α-synuclein seed amplification assay in Alzheimer's disease neuroimaging initiative: Prevalence and associations with Alzheimer's disease biomarkers and cognitive function
- The Inflammatory Marker YKL-40 Is Elevated in Cerebrospinal Fluid from Patients with Alzheimer's but Not Parkinson's Disease or Dementia with Lewy Bodies
- A digital biomarker of white-matter routing from diffusion MRI as an early biomarker of Alzheimer’s disease
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 →