Multiple biological pathways are altered and could be targeted very early in the Alzheimer's continuum. 1 key finding →
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.
Our results demonstrate that novel AD biomarker candidates are identified and confirmed by proteomic studies of brain tissue and biofluids, providing a rich resource for large-scale biomarker validation for the AD community. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The relationship between amyloid-β (Aβ) species and tau pathology in Alzheimer's disease (AD) is not fully understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial Alzheimer's disease (fAD) mutations alter amyloid precursor protein (APP) cleavage by γ-secretase, increasing the proportion of longer amyloidogenic amyloid-β (Aβ) peptides. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid precursor protein (APP) mutations associated with familial Alzheimer's disease (AD) usually lead to increases in amyloid β-protein (Aβ) levels or aggregation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma Aβ measures may be useful biomarkers for predicting cerebral Aβ and tau. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Because they have a high prevalence of several common diseases and chronic conditions, Danish centenarians are not healthy. 1 key finding →
Participants: 276 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma levels of Aβ oligomers could be assessed using MDS, which might be a simple, noninvasive, and accessible assay for evaluating brain amyloid deposition related to AD pathology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Circulating long noncoding RNAs (lncRNAs) might serve as biomarkers for different pathological conditions. 5 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood biomarkers have emerged as accessible, cost-effective, and highly promising tools for advancing the diagnostics of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
While blood-based tests are readily available for various conditions, including cardiovascular diseases, type 2 diabetes, and common cancers, Alzheimer's disease (AD) and other neurodegenerative diseases lack an early blood-based screening test that can be used in primary care. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The combination BBBM with MMSE is projected to increase the efficiency and value of the triage process for DMT eligibility. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma Aβ ratios in this study are a potential biomarker for brain Aβ deposition and therefore, for preclinical AD. 2 key findings →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
In summary, specific biomarkers for AD-related pathologies allow accurate clinical diagnosis of AD based on pathobiological parameters. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Biological aging is the correlated decline of multi-organ system integrity central to the etiology of many age-related diseases. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The primary Aβ-based blood biomarker funnels individuals with suspected AD for subsequent validation of the diagnosis by structure-based combined analysis of the CSF biomarkers Aβ and tau. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Phosphorylated-tau 217 (pTau217) is currently the most promising blood-based biomarker for accurately detecting Alzheimer's disease (AD) pathology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The plasma p-tau217 and plasma GFAP models adequately predicted the change over time, with donanemab resulting in decreased plasma p-tau217 and plasma GFAP concentrations. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) presents a critical global challenge, accounting for over 60 % of the 57 million current dementia cases worldwide, with prevalence projected to exceed 100 million by 2050. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
No significant differences in p-tau217, GFAP and NfL level were observed between groups (pFDR > 0.08). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Validated plasma phosphorylated tau 217 (p-tau217) assays identify Alzheimer disease pathology with high accuracy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) measures of phosphorylated-tau (P-tau) 231 and P-tau181 are two biomarkers for the identification of tau pathology as related to Alzheimer's disease (AD). 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
It is unclear whether Alzheimer disease pathology drives cognitive decline in Parkinson disease (PD) patients carrying GBA1 variants. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease(AD) is being the burden of society and family. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Patients were followed for a median of 2.92 years. 5 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 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 →