Increasing variation greatly impacted the performance of plasma Aβ42/40 in discriminating Aβ status. 1 key finding →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
55/100
In Alzheimer's diseases (AD), tau pathology is strongly associated with cognitive decline. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Centrifugation improved the performance of plasma p-tau217, but thawing temperatures and up to three freeze-thaw cycles did not have a significant impact. 5 key findings →
Participants: 50 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Despite reductions in plasma p-tau217 with donanemab treatment, this biomarker cannot currently be used to accurately detect TRAC by PET (< 24.1 CL) in individuals with early symptomatic AD. 1 key finding →
Design: phase-3-trial Participants: 830 Evidence: null result
Full summary, score breakdown and related studies → Original source Free full text
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
Alzheimer's disease (AD) neuropathology is associated with neuroinflammation, but there are few useful biomarkers. 4 key findings →
Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
53/100
Tau is a hallmark pathology of Alzheimer's disease, and animal models have suggested that tau spreads from cell to cell through neuronal connections, facilitated by β-amyloid (Aβ). 3 key findings →
Participants: 312 Evidence: low
Full summary, score breakdown and related studies → Original source
A growing body of evidence suggests that the dysregulation of neuronal iron may play a critical role in Alzheimer's disease. 3 key findings →
Participants: 236 Evidence: low
Full summary, score breakdown and related studies → Original source
In this patient, the clinical disease symptoms progressed rapidly in life, paralleled with an annual increase of tau PET retention of 20% to 40% in many cortical regions. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation may be involved in the pathophysiology of Parkinson's disease (PD) and specifically in non-motor symptoms such as depression, fatigue and cognitive impairment. 4 key findings →
Participants: 87 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We examined whether plasma p-tau181 and p-tau217 are specific biomarkers of pathologically confirmed Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
51/100
Alzheimer's Disease Neuroimaging Initiative database. 4 key findings →
Participants: 57 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that, among PSEN1 mutation carriers, females had a greater rate of neurodegeneration than males, yet it did not predict cognitive performance. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammation has been implicated in the pathogenesis of Parkinson's disease (PD). 4 key findings →
Participants: 131 Evidence: low
Full summary, score breakdown and related studies → Original source
A major difference in the revised diagnostic criteria for Alzheimer's disease (AD) is the incorporation of biomarkers to support a clinical diagnosis and allow the identification of preclinical AD due to AD neuropathological processes. 5 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
50/100
Recent findings show that structural network topology is disrupted in Alzheimer's disease (AD), with changes occurring already at the prodromal disease stages. 2 key findings →
Participants: 299 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The extent to which newly developed blood-based biomarkers could reduce screening costs in secondary prevention trials of Alzheimer's disease is mostly unexplored. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic pathways implicated in causing AD are related to altered levels of soluble tau through both Aβ-dependent and Aβ-independent mechanisms, which may have relevance for anti-tau drug development. 3 key findings →
Participants: 751 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is an urgent need for biomarkers in plasma to identify Alzheimer's disease (AD). 3 key findings →
Participants: 142 Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
The National Institute on Aging and the Alzheimer's Association convened three separate work groups in 2011 and single work groups in 2012 and 2018 to create recommendations for the diagnosis and characterization of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The choice of tau biomarker may differ by disease stage and research goals that seek to maximize sensitivity or specificity. 2 key findings →
Participants: 351 Evidence: low
Full summary, score breakdown and related studies → Original source
A highly robust assay for repeatedly measuring Abeta forms in plasma such as INNO-BIA plasma Abeta forms might be a useful tool in a future risk assessment of AD. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
Mixed pathologies of α-synuclein, β-amyloid and tau are relatively common in Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB). 5 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid synaptotagmin-1 is a promising biomarker to monitor synaptic dysfunction and degeneration in Alzheimer's disease that may be useful for clinical diagnosis, to monitor effect on synaptic integrity by novel drug candidates, and to explore pathophysiology directly in patients with Alzheimer's disease. 3 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
We constructed a standardized operating procedure for plasma handling, to facilitate introduction of blood-based biomarkers into the research and clinical settings. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,040 records (3.4% of the library) are not peer-reviewed — 965 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events