Patients with ADRD (n = 1,525, 24.8%) were less likely to have recorded severe pain than others (16.4% vs. 23.6%, p < .001). 4 key findings →
Participants: 1,525 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.
55/100
Five phenotypes were identified: (1) comorbid ischemic heart disease with hospitalization and skilled nursing facility use (22% of the HN sample), (2) comorbid ischemic heart disease with home care use (23%), (3) home care use (12%), (4) high comorbidity with hospitalization (32%), and (5) Alzheimer's disease/related dementias with functional dependency and nursing home use (11%). 4 key findings →
Design: cross-sectional Participants: 415 Evidence: low
Full summary, score breakdown and related studies → Original source
Costs/follow-up day distributions differed significantly across cognitive categories. 5 key findings →
Participants: 3,545 Evidence: low
Full summary, score breakdown and related studies → Original source
KmL identified 2 distinct Dependence Scale clusters: (A) high initial dependence, faster decline, and (B) low initial dependence, slower decline. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
These longitudinal estimates clarify the sequence and temporal dynamics of presymptomatic pathologic changes in autosomal dominant AD, information critical to a better understanding of the disease. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma a-synuclein level was significantly increased in patients with PD and APS when compared with controls and FTD without parkinsonism (p<0.01). 5 key findings →
Participants: 204 Evidence: low
Full summary, score breakdown and related studies → Original source
Although a small-scale study (n = 60), it suggests that older adults operate in larger geographic spaces than in the areas where they reside. 5 key findings →
Design: cross-sectional Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The volume of the hippocampal formation predicted performance on most acquisition and recall measures across the spectrum of normal aging and AD. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Crenezumab is a humanized anti-abeta monoclonal antibody in development for the treatment of Alzheimer disease (AD). 5 key findings →
Design: clinical trial Participants: 433 Evidence: high
Full summary, score breakdown and related studies → Original source
SCarlet RoAD (NCT01224106; WN25203), a Phase 3, multicenter, randomized, double-blind, placebo-controlled, 2-year study of gantenerumab in prodromal AD, was the first global registration-enabling study using biomarker screening for entry and a single clinical endpoint for outcome. 3 key findings →
Design: clinical trial Participants: 312 Evidence: high
Full summary, score breakdown and related studies → Original source
55/100
Baseline demographics were similar between the treatment groups. 5 key findings →
Participants: 144 Evidence: high
Full summary, score breakdown and related studies → Original source
There were no group differences with any of the outcome measures in an intent-to-treat analysis. 5 key findings →
Participants: 41 Evidence: high
Full summary, score breakdown and related studies → Original source
The mean age of the participants was 70 years, and 55% were male. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
46 (4.7%) subjects were classified as having probable or possible Alzheimer's disease. 5 key findings →
Participants: 980 Evidence: low
Full summary, score breakdown and related studies → Original source
G) Functions, such as vessel stabilization, regulation of vascular tone and maintenance of local and tissue homeostasis (contractile capacity and vessel permeability regulation), matrix protein synthesis, macrophage-like properties, immunological defense, intervention in coagulation, participation in mechanisms that regulate the quiescent and angiogenic stages of blood vessels (including the behaviour of pericytes during sprouting angiogenesis and intussuceptive vascular growth, as well as pericyte interactions with endothelium and other cells, and with extracellular matrix) and plasticity, as progenitor cells with great mesenchymal potential, originating other pericytes, fibroblast/myofibroblasts, preadipocytes, chondroblasts, osteoblasts, odontoblasts, vascular smooth muscle and myointimal cells. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Misidentification, wandering or agitation, and physical aggression increased during follow-up. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
There was a significant intervention effect as hypothesized for participants with lower mastery at baseline on all three bother (p =.04), anxiety (p =.01), and depression (p =.007). 4 key findings →
Design: longitudinal study Evidence: high
Full summary, score breakdown and related studies → Original source
Increased p-tau181 was observed for both ɛ4 carriers and non-carriers close to AD onset, but exclusively for ɛ4 carriers in the early preclinical groups (7- and 13-years pre-AD). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Baseline plasma NfL was a significant predictor of psychotic symptoms longitudinally across the study adjusted for age, Hoehn and Yahr stage, duration of follow up, duration of disease, baseline levodopa and dopamine agonist medication, and baseline cognition: (OR 8.15 [95% CI 1.40–47.4], p = 0.020). 5 key findings →
Participants: 63 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Galectin-3 (Gal-3) is a beta-galactosidase binding protein involved in microglial activation in the central nervous system (CNS). 5 key findings →
Participants: 119 Evidence: low
Full summary, score breakdown and related studies → Original source
55/100
Models integrating pTau217R outperformed Aβ42/Aβ40 alone, predicting amyloid levels up to 89.1 CL. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We provide evidence that increased CSF sPDGFRβ is associated with BBB leakage in the early cognitive impairment stage of AD, which may contribute to cognitive impairment in AD progression. 5 key findings →
Participants: 158 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The sensitive NULISA multiplex approach supports differential diagnosis and target identification, with prognostically informative dementia-related biomarkers. 5 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source
The associations of synaptic loss with amyloid-β (Aβ) and tau pathology measured by positron emission tomography (PET) and plasma analysis in Alzheimer's disease (AD) patients are unknown. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our study confirms a lack of suitability of CSF C3 and FH as diagnostic biomarkers of AD, but points to their modest potential as prognostic biomarkers and therapeutic targets in cognitively impaired patients. 2 key findings →
Design: longitudinal study Evidence: moderate
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 →