The prevalence of PIMcogs increased from 16% at baseline to 23% at follow-up. 5 key findings →
Participants: 397 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
In the MCI+NPS group, the most frequently endorsed NPS was anxiety (46.2 %), the less prevalent NPS was euphoria/elation (1.44 %). 5 key findings →
Design: cross-sectional Participants: 376 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
All included PD patients were cognitively normal at baseline and had 6 years of follow-up assessments available for cognitive status. 5 key findings →
Design: longitudinal study Participants: 47 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 558 amnestic MCI participants (168 ChEI users), ChEI users exhibited higher risk of progression to AD dementia (hazard ratio = 1.77, 95% confidence interval: 1.15 to 2.73, p = 0.001). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
< 0.001). Shape features demonstrated the highest predictive accuracy for conversion, with areas under the curve of 0.891 at baseline and 0.898 at 2 years. 5 key findings →
Design: longitudinal study Participants: 180 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The PD-MCI nonreversion group had greater p-tau:amyloid beta and t-tau:amyloid beta ratios relative to the PD-MCI reversion group. 4 key findings →
Design: longitudinal study Participants: 430 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Thirteen studies were included (five guidelines, two clinical decisions, two systematic reviews, one meta-analysis, and three RCTs). 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Disruptions in GABAergic activity and alterations in gamma oscillations are key pathological features of AD associated with amyloid-beta (Aβ) plaques. 3 key findings →
Design: longitudinal study Participants: 127 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our results highlight the prognostic value of biological AD staging. 5 key findings →
Participants: 492 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Real tACS paired with cognitive exercises significantly improved ADAS-Cog scores post-treatment compared to pre-treatment (p-value = 0.019), whereas sham tACS did not. 5 key findings →
Participants: 42 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Soluble N-ethylmaleimide-sensitive factor attachment proteins receptors (SNARE) proteins, such as VAMP-2 and SNAP-25, are implicated in α-synuclein pathophysiology and CSF levels of these proteins are associated with pathophysiological biomarkers and cognitive decline in Alzheimer’s disease (AD). 5 key findings →
Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
After adjusting for potential confounders, multivariable logistic regression models revealed that the prevalence of dementia was significantly higher in individuals with chronic pain than in those without. 3 key findings →
Design: cross-sectional Participants: 1,096 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this retrospective, confounder-adjusted study, anticoagulation was associated with slower cognitive/functional decline and lower hospitalization/mortality risk in AF and dementia patients. 3 key findings →
Design: cohort study Participants: 291 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Over a median follow-up period of 4.33 years, 637 participants (7.27%) developed dementia. 5 key findings →
Design: longitudinal study Participants: 8,758 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
During follow-up, cholinergic WMHV was associated with an annual decline of Mini-Mental State Examination (MMSE) (β coefficient, -0.239; P = 0.004), and incident dementia (HR = 3.54; 95%CI: 2.05-6.10). 5 key findings →
Design: cross-sectional Participants: 751 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
36.5% of the overall cohort experienced delirium. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Odds ratios for death, dementia, and delirium using anticholinergic-polypharmacy pseudoscales (median = 1.09-1.10) were greater than those of general-polypharmacy pseudoscales (1.05-1.06). 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
49/100
Of 164,508 eligible participants, 6605(4%) had cognitive testing scores consistent with MCI. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
49/100
Aggregated TDP-43 is a hallmark of frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), and limbic-predominant age-related TDP-43 encephalopathy (LATE), and a common co-pathology in other neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The FCAAS-4 achieved a mean area under the receiver operating characteristic curve (AUC-ROC) of 0.74 (95% confidence interval: 0.71-0.77) and a Harrell generalized c-index of 0.72 (0.70-0.75). 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The study included 25 patients with iCAA (age, 44±11 years), 31 patients with sCAA (age, 75±5 years), 28 patients with AD (age, 71±8 years) and 30 controls (age, 72±8 years) from 9 case descriptions and 1 cohort study. 5 key findings →
Design: cohort study Participants: 25 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
= 0.015). In this autopsy-confirmed cohort, seizure susceptibility was associated with advanced tau pathology and CAA in AD. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Recent advances in our understanding of non-cell-autonomous mechanisms in neurodegenerative diseases (NDDs) have highlighted microglial dysfunction as a core driver of disease progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In AD cases, pTau181 and ApoE4 levels were elevated, and the Aβ1-42/1-40 ratio was reduced. 5 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
They remain a significant focus of scientific and clinical interest due to their increasing medical and social importance. 2 key findings →
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 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 →