No significant disparities in plasma ubiquitin levels for various levels of cognitive functioning were identified. 5 key findings →
Participants: 230 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.
Twenty-nine percent of the cohort had Montreal Cognitive Assessment (MoCA) scores indicative of cognitive impairment or dementia after adjusting for age, sex, and education based on National Alzheimer's Coordinating Center normative data. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
There were significant differences in plasma p‐tau181 values between Controls and those with AD at all ages up to 85 years. 5 key findings →
Participants: 1,558 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p‐tau181 differentiated pathology‐confirmed AD from NC with negative amyloid PET scans with an AUC of 0.93. 5 key findings →
Participants: 91 Evidence: moderate
Full summary, score breakdown and related studies → Original source
BBBO was achieved in 5 out of 6 subjects with an average volume of 983 ± 626 mm 3 following FUS at the right frontal lobe both in white and gray matter regions. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
It is unknown how neuroinflammation may feature in the etiology of Alzheimer's disease (AD). 1 key finding →
Participants: 1,291 Evidence: low
Full summary, score breakdown and related studies → Original source
Linear models showed that plasma GFAP was significantly higher in αSyn+AD compared to αSyn (β = 0.31, 95% CI = 0.065-0.56, and P = 0.015), after covarying for age at plasma, plasma-to-death interval, and sex; plasma p-tau 181 was not (P = 0.37). 4 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest that, among PSEN1 mutation carriers, females had a greater rate of neurodegeneration than males, yet it did not predict cognitive performance. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
In cognitively unimpaired adults, elevated plasma p-tau181 is associated with future increased Aβ deposition across multiple brain regions. 5 key findings →
Participants: 18 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the primary type of dementia, followed by frontotemporal lobar degeneration (FTLD). 1 key finding →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
The decrease of Ruminococcaceae and the increase of Megamonas could act as predictive markers for the rapidly progressive MCI. 4 key findings →
Participants: 1,013 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggest that although WMH are primarily related to systemic vascular risk and neurodegeneration (i.e., t-tau), AD-specific pathways may contribute to the formation of WMH in a regionally-specific manner, with neurofibrillary tangles (i.e., p-tau) playing a role in temporal WMHs and amyloid (i.e., Aβ 42/Aβ 40) in parietal WMHs. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammation has been implicated in the pathogenesis of Parkinson's disease (PD). 4 key findings →
Participants: 131 Evidence: low
Full summary, score breakdown and related studies → Original source
ADNI has had a profound impact in improving clinical trials for AD. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
A connection between dementias and blood-brain barrier (BBB) dysfunction has been suggested, but previous studies have yielded conflicting results. 2 key findings →
Participants: 130 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A major difference in the revised diagnostic criteria for Alzheimer's disease (AD) is the incorporation of biomarkers to support a clinical diagnosis and allow the identification of preclinical AD due to AD neuropathological processes. 5 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
This study tests the hypothesis that GM and mediators of the microbiota-gut-brain axis (MGBA) are associated with the amyloid cascade in sporadic AD. 5 key findings →
Participants: 34 Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammatory markers have been shown to predict neurocognitive outcomes in aging adults; however, the degree to which peripheral markers mirror the central nervous system remains unknown. 5 key findings →
Participants: 173 Evidence: moderate
Full summary, score breakdown and related studies → Original source
αSyn-PMCA is almost invariably positive in the CSF of patients with PAF establishing this condition as α-synucleinopathy. 1 key finding →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
The present data indicate that CSF NfL and t-tau levels reflect distinct pathophysiological mechanisms of neurodegeneration and support the clinical use of NfL as a fast screening biomarker for the differential diagnosis of atypical/rapidly progressive NDs. 4 key findings →
Participants: 141 Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes play a formative role in memory consolidation during physiological conditions; when dysregulated, astrocytes release glial fibrillary acidic protein (GFAP), which has been linked with negative memory outcomes in animal studies. 3 key findings →
Participants: 69 Evidence: low
Full summary, score breakdown and related studies → Original source
Increased NFL levels are a common feature in neurodegenerative dementias. 2 key findings →
Participants: 122 Evidence: low
Full summary, score breakdown and related studies → Original source
50/100
Recent findings show that structural network topology is disrupted in Alzheimer's disease (AD), with changes occurring already at the prodromal disease stages. 2 key findings →
Participants: 299 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results provide support for the continued study of plasma biomarkers as a clinical screening tool for AD and VCID pathology. 4 key findings →
Participants: 90 Evidence: low
Full summary, score breakdown and related studies → Original source
The MMSE score, MoCA score, serum miR-27a-3p level, cerebrospinal fluid miR-27a-3p, Aβ42 levels and Aβ42/Aβ40 ratio of AD patients in mild group and moderate-to-severe group were all lower than those in the control group, and the moderate-to-severe group were lower than the mild group (all P < 0.05);the serum NEAT1 level, SUVR, and cerebrospinal fluid NEAT1 and BACE1 levels were higher than those in the control group, and the moderate-to-severe group were higher than the mild group (all P < 0.05). 1 key finding →
Participants: 41 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 →