Vascular contributions to dementia and Alzheimer's disease are increasingly recognized 1-6 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease is an incurable neurodegenerative disorder in which neuroinflammation has a critical function 1 . 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
47/100
Defective brain hormonal signaling has been associated with Alzheimer's disease (AD), a disorder characterized by synapse and memory failure. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The current study tested the accuracy of primary MRI and cerebrospinal fluid (CSF) biomarker candidates and neuropsychological tests for predicting the conversion from mild cognitive impairment (MCI) to Alzheimer's disease (AD) dementia. 1 key finding →
Participants: 81 Evidence: low
Full summary, score breakdown and related studies → Original source
Subjects with mild cognitive impairment (MCI) are at a high risk of developing clinical Alzheimer's disease (AD). 2 key findings →
Participants: 52 Evidence: low
Full summary, score breakdown and related studies → Original source
This study revealed that exosomal GAP43, neurogranin, SNAP25, and synaptotagmin 1 act as effective biomarkers for prediction of AD 5 to 7 years before cognitive impairment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The authors propose that axonal damage markers in CSF may discriminate between subtypes of ALS and that they could be used as markers for therapeutic trials. 1 key finding →
Participants: 69 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid from 70 patients with Alzheimer's disease (AD) and 96 patients with non-AD neurological diseases as well as 19 normal control subjects was surveyed by sandwich enzyme-linked immunosorbent assay to quantitate levels of the microtubule-associated protein tau in cerebrospinal fluid. 3 key findings →
Participants: 70 Evidence: low
Full summary, score breakdown and related studies → Original source
Imaging and CSF biomarkers can improve prediction of conversion from MCI to AD compared with baseline clinical testing. 3 key findings →
Participants: 97 Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenic mechanisms of Alzheimer's disease (AD) remain largely unknown and clinical trials have not demonstrated significant benefit. 5 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
Prediction of conversion from mild cognitive impairment (MCI) to Alzheimer's disease (AD) is of major interest in AD research. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
46/100
Alzheimer disease (AD) is multi-factorial and heterogeneous. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The microtubule-associated tau protein abnormally phosphorylated at threonine 231 (p-tau231) has been investigated as a potential marker of Alzheimer disease. 4 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Protein kinase B (PKB) is an important intermediate in the phosphatidylinositol-3 kinase signaling cascade that acts to phosphorylate glycogen synthase kinase-3 (GSK-3) at its serine 9 residue, thereby inactivating it. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The purpose of this study was to investigate the potential relationships between cerebrospinal fluid (CSF) measurements of beta-amyloid-1-42 (Abeta(1-42)) and total tau to (11)C-Pittsburgh compound B ((11)C-PiB) and 2-(1-{6-[(2-(18)F-fluoroethyl)(methyl)amino]-2-naphthyl}ethylidene) malononitrile ((18)F-FDDNP) binding as measured using PET. 4 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
46/100
Therapies designed to decrease the level of SOD1 are currently in a clinical trial for patients with superoxide dismutase (SOD1)-linked familial amyotrophic lateral sclerosis (ALS). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Individuals with Down's syndrome (DS) develop early Alzheimer's disease (AD) with β-amyloid (Aβ) plaque pathology. 4 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
46/100
One-hundred nineteen individuals with a family history of AD (Presymptomatic Evaluation of Experimental or Novel Treatments of Alzheimer's Disease [PREVENT-AD] cohort, mean age 67 ± 5 years) underwent tau-PET ([ 18 F]FTP), β-amyloid (Aβ)-PET ([ 18 F]NAV4694 [NAV]), and cognitive assessment. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Biomarkers are needed to improve the sensitivity and accuracy of diagnosis, and also prognosis, in individuals with early Alzheimer disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neuraminidase 1 (NEU1) cleaves terminal sialic acids from sialoglycoproteins in endolysosomes and at the plasma membrane. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
46/100
Concentrations of phosphorylated tau181, total tau (t-tau), and β-amyloid in the CSF were measured in 3 groups: 22 former professional athletes with multiple concussions (mean ± SD age 55.9 ± 12.2 years), 5 healthy controls (age 57.4 ± 5.2 years), and 12 participants (age 60.0 ± 6.6 years) diagnosed with Alzheimer disease (AD). 4 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Extracellular plaques composed of the hydrophobic peptide amyloid-β and intraneuronal accumulation of the hyperphosphorylated protein tau (p-tau) are pathological hallmarks found in the brains of most people affected by Alzheimer's disease (AD). 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Poor subjective sleep quality is linked to reduced brain volume and cortical thickness (CTh), but associations with objective sleep measures, particularly regarding sex and AD pathology, remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
No amyloid-related imaging abnormalities occurred. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A higher DMV score was significantly associated with increased likelihoods of MCI (OR=1.19; 95%CI=1.06‒1.34) and amnestic mild cognitive impairment (aMCI) (1.21; 1.06‒1.37), and lower scores in MMSE (-0.01; -0.02‒0.00; p = 0.041), global cognition (-0.05; -0.08‒-0.03), memory (-0.06; -0.10‒-0.02), verbal fluency (-0.05; -0.08‒-0.02), attention (-0.04; -0.07‒-0.01), and executive function (-0.06; -0.10‒-0.03). 3 key findings →
Design: cross-sectional Participants: 903 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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