43/100
Plasma p-tau231 showed a significant rate of change over time. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurovascular unit (NVU) inflammation via activation of glial cells and neuronal damage plays a critical role in neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Major depressive disorder (MDD) is a prevalent brain disorder affecting more than 2% of the world's population. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers represent promising tools for the screening and diagnosis of patients with neurodegenerative conditions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurological damage is the pathological substrate of permanent disability in various neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Emerging evidence suggests that repetitive negative thinking (RNT; i.e., worry and ruminative brooding) is associated with biomarkers of Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent technological advances have improved the sensitivity and specificity of blood-based biomarkers for Alzheimer's disease and related dementias. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative disorders such as Alzheimer's disease (AD) represent an increasingly significant public health concern. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia is a group of symptoms including memory loss, language difficulties, and other types of cognitive and functional impairments that affects 57 million people worldwide, with the incidence expected to double by 2040. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-β (Aβ)42 and arterial calcification were associated with cognitive performance. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glutamate transporter-1 (GLT-1) dynamics are implicated in excitotoxicity and Alzheimer's disease (AD) progression. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This commentary focuses on the clinical utility of plasma amyloid-β (Aβ) 42/40 to detect semantic intrusion errors in amnestic mild cognitive impairment, as investigated Curiel Cid et al. in a recent issue of the Journal of Alzheimer's Disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) involves reduced glutathione levels, causing oxidative stress and contributing to neuronal cell death. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid beta (Aβ) 42/40 ratio has been widely studied as a biomarker in Alzheimer's disease (AD); however, other Aβ peptides could also represent relevant biomarkers. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The hAβ-KI and APPSAA-KI are two amyloid models that harbor mutations in the endogenous mouse App gene. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Age-associated cerebral small vessel disease (CSVD) represents a clinically heterogenous condition, arising from diverse microvascular mechanisms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent research has linked systemic metabolic disorders to cognitive decline and dementia risk, including Alzheimer's. This is suspected to be due to lifestyle-related vascular impairments from atherosclerosis and other factors, such as malnutrition and anaemia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Medical science has made revolutionary discoveries around the nosology and aetiology of the neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia represents a growing public health burden with large social, racial, and ethnic disparities. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ethics Review began a decade ago with a mission to identify ethical concerns that hold back innovation and to promote solutions that would move the field forward. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a serious dementia afflicting aging population and is characterized by cognitive decline, amyloid-β plaques, and neurofibrillary tangles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood biomarkers are minimally invasive, are available at a relatively low cost, and are easily accessible; therefore, they are expected to play a pivotal role in the diagnosis of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative dementias and related diseases, such as Alzheimer's disease, dementia with Lewy bodies, and Parkinson's disease have no fundamental cure yet. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Cerebrospinal fluid (CSF) biomarkers are currently the only clinically validated biofluid diagnostic test for Alzheimer's Disease (AD) available in Australia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The synaptic proteins revealed no statistically significant differences between BD and HC, neither at baseline, one-year follow-up, or in terms of changes from baseline to follow-up. 4 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →