41/100
Hyperhomocysteinemia is recognized as a risk factor for several diseases, including cardiovascular and neurological conditions. 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 findings highlight sexual dimorphism in the behavior, neuropathology, and plasma proteins in tau P301S transgenic AD mice, indicating that the use of male P301S transgenic mice may be more suitable for assessing anti-phosphorylated tau therapeutic strategies for AD and related tauopathies, and the MIP-3α may be a new potential plasma biomarker. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The overlapping symptoms of behavioural variant frontotemporal dementia (bvFTD) and primary psychiatric disorders (such as depressive disorder, schizophrenia spectrum, and bipolar disorder) present a challenge for the differential diagnosis of bvFTD in middle and older-aged people. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a progressive neurodegenerative disorder, with the strongest disease-associated changes observed at clinical or end-stage disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers represent a less invasive and potentially cheaper approach for aiding Alzheimer's disease (AD) detection compared with cerebrospinal fluid and some neuroimaging biomarkers. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-isolated BEVs have emerged as a novel player in the study of AD, with enormous potential as a diagnostic, evaluation of therapeutics, and treatment tool. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accurate identification of Alzheimer's disease (AD) is still of major clinical importance considering the current lack of noninvasive and low-cost diagnostic approaches. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of neurodegenerative dementia and there is no cure to date. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral deposition of the beta-amyloid peptide (A beta) is an invariant feature of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The 4-kilodalton (39 to 43 amino acids) amyloid beta protein (beta AP), which is deposited as amyloid in the brains of patients with Alzheimer's diseases, is derived from a large protein, the amyloid beta protein precursor (beta APP). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A beta 1-40, a major component of Alzheimer's disease cerebral amyloid, is present in the cerebrospinal fluid and remains relatively soluble at high concentrations (less than or equal to 3.7 mM). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The possibility that hypersecretion of corticotropin-releasing factor (CRF) contributes to the hyperactivity of the hypothalamo-pituitary-adrenal axis observed in patients with major depression was investigated by measuring the concentration of this peptide in cerebrospinal fluid of normal healthy volunteers and in drug-free patients with DSM-III diagnoses of major depression, schizophrenia, or dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
See Mander et al. (doi:10.1093/awx174) for a scientific commentary on this article. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The accumulation in brain of senile plaques containing beta-amyloid protein (A beta) is a defining feature of Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) lacks protein biomarkers reflective of its diverse underlying pathophysiology, hindering diagnostic and therapeutic advancements. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Groups of patients with idiopathic Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy or Steele-Richardson-Olszewski syndrome, matched for overall clinical disability, were compared using three computerised cognitive tests previously shown to be sensitive to frontal lobe dysfunction. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggest that cognitive benefits of bariatric surgery may extend to 24-months postoperatively. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Mild cognitive impairment (MCI), an identified prodromal stage of Alzheimer's Disease (AD), often evades detection in the early stages of the condition, when existing diagnostic methods are employed in the clinical setting. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Coronavirus Disease 2019 (COVID-19) pandemic-triggered mortality is significantly higher in older than in younger populations worldwide. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Modest relationships were seen between mean VPC novelty preference and the PACC (r=.39, P=.007) and NIHTB-CB (r=.35, P=.03) composite scores, and additional individual neurocognitive task scores including letter fluency (r=.33, P=.02), category fluency (r=.36, P=.01), and Trail Making Test A (-.40, P=.006). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The positive results pave the way for the deployment of the system to a nonsupervised environment, thus representing a potential efficacious and ecological solution to support clinicians in the identification of early signs of cognitive decline. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Due to the lack of pharmacological treatment for dementia, timely detection of subjects at risk can be of seminal importance for preemptive rehabilitation interventions. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dorsiflexion ROM limitation is associated with ankle injuries, foot pain, lower limb disorders, loss of balance, gait control disorders and fall risk in older adults. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Preclinical AD risk, defined as possessing at least one APOE ε4 allele, is not only associated with mean-level performance differences, but also with increases in variability across repeated testing occasions particularly on a test of processing speed. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Smartphones and wearables could provide beneficial and pervasive support and monitoring for rehabilitation among people with dementia. 3 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 →