The co-occurrence of Aβ and ND accelerates cognitive decline in CN individuals. 4 key findings →
Design: longitudinal study Evidence: moderate
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.
An accurate description of changes in the brain in healthy aging is needed to understand the basis of age-related changes in cognitive function. 3 key findings →
Design: cross-sectional Participants: 122 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Atraumatic convexal subarachnoid hemorrhage (cSAH) in elderly patients is a rare entity that has been associated with cerebral amyloid angiopathy (CAA) and intracerebral hematomas (ICH). 5 key findings →
Design: cohort study Participants: 22 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Preclinical evidence in transgenic models of Alzheimer's disease suggests that liraglutide exerts neuroprotective effects by reducing amyloid oligomers, normalising synaptic plasticity and cerebral glucose uptake, and increasing the proliferation of neuronal progenitor cells. 4 key findings →
Participants: 206 Evidence: high
Full summary, score breakdown and related studies → Original source
Brain aging is accompanied by patterns of functional and structural change. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
59/100
Alzheimer's Disease (AD) is one of the leading causes of death in developed countries. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 239 participants underwent blood draw and Aβ-PET (age 70.8 ± 7.8, 55.2% female, education 15.6 ± 3.4 years, 48.9% Hispanic/Latino, 94.9% white). 5 key findings →
Participants: 239 Evidence: low
Full summary, score breakdown and related studies → Original source
Greater multimorbidity burden was associated with worse cognition and biomarkers of AD (PET amyloid standardized uptake value ratios and positivity, p-tau181, and p-tau217), neurodegeneration (neurofilament light, total tau, cortical thickness, and hippocampal volume), and SVD (white matter hyperintensity volume and presence of lacune and cerebral microbleeds). 3 key findings →
Participants: 3,808 Evidence: low
Full summary, score breakdown and related studies → Original source
Virtually identical t-tau/Aβ42 cut-points (∼0.54) performed best in both test cohorts and with similar accuracy (areas under ROC curve [AUCs] [A/B: 0.95; C: 0.94]). 3 key findings →
Participants: 138 Evidence: moderate
Full summary, score breakdown and related studies → Original source
59/100
Three genome-wide significant associations were identified for p-tau181: TUBAP/rs76523946, P = 2.21E-08; CTNND2/rs142510573, P = 3.04E-08; CLSTN2/rs112448655, P = 3.04E-08, and one for t-tau (JHY/rs77264104, P = 2.84E-08). 5 key findings →
Participants: 375 Evidence: moderate
Full summary, score breakdown and related studies → Original source
[18F]Flutemetamol and [18F]florbetaben data demonstrated an increased bias in amyloid estimate for larger intervals and higher noise levels. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Positron emission tomography (PET)-based staging of regional amyloid deposition has recently emerged as a promising tool for sensitive detection and stratification of pathology progression in Alzheimer's Disease (AD). 2 key findings →
Design: cross-sectional Participants: 403 Evidence: moderate
Full summary, score breakdown and related studies → Original source
59/100
DL-ADprob was independently prognostic in both ADNI-MCI (P < .001) and HABS-CU (P = .048) sets. 5 key findings →
Participants: 1,050 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a global healthcare challenge lacking a simple and affordable detection method. 3 key findings →
Participants: 1,671 Evidence: low
Full summary, score breakdown and related studies → Original source
59/100
Metabolically healthy obese (MHO) individual is known to be defended from the metabolic complications of obesity. 2 key findings →
Design: cross-sectional Participants: 171 Evidence: low
Full summary, score breakdown and related studies → Original source
Brain amyloid deposition is thought to be a seminal event in Alzheimer’s disease. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Longitudinal OEF change in older adults is primarily related to vascular pathology. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Including apolipoprotein E-ε4 (APOE-ε4) status and older age into consideration may increase the accuracy of plasma Aβ 42 /Aβ 40 detecting Aβ+ individuals, but the rationale behind this remains to be fully understood. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
There are biologically meaningful Aβ-downstream effects in individuals with a low burden of Aβ pathology, while structural and functional changes are still subtle or absent. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid PET results were positive for 242 patients (48%). 4 key findings →
Participants: 866 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
CSF synaptic biomarkers increase in the early preclinical stages of the Alzheimer continuum even when a low burden of Aβ pathology is present, and they differ in their association with age, sex, APOE ε4 , and markers of neurodegeneration. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Data-driven WMH spatial patterns reflect discrete underlying etiologies including arteriolosclerosis, CAA, AD, and normal aging. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
58/100
Accounting for educationalfactors, vascular factors, and Aβ burden diminished, but did not eliminate, racial differences in PACC5 performance longitudinally. 4 key findings →
Design: longitudinal study Participants: 296 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The proposed novel, pragmatic method to determine CSF biomarker cutoffs for AD does not require assessment of other biomarkers or assumptions concerning the clinical diagnosis of patients. 1 key finding →
Participants: 497 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
58/100
Longitudinal racial differences in amyloid biomarkers are observed. 1 key finding →
Design: longitudinal study Participants: 179 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
9 of the 2,925 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.
- Cerebral small vessel disease unveils a vascular pathway to motoric cognitive risk in aging
- Progressive logopenic/phonological aphasia: erosion of the language network
- Baseline and longitudinal increases in diastolic blood pressure are associated with greater white matter hyperintensity volume: the northern Manhattan study
- Associations of CSF PDGFRβ With Aging, Blood-Brain Barrier Damage, Neuroinflammation, and Alzheimer Disease Pathologic Changes
- One-Stop Shop: 18F-Flortaucipir PET Differentiates Amyloid-Positive and -Negative Forms of Neurodegenerative Diseases
- The Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging: methodology and baseline characteristics of 1112 individuals recruited for a longitudinal study of Alzheimer's disease
- Chronology and Chronicity of Altered Resting-State Functional Connectivity after Traumatic Brain Injury
- Change in rates of cerebral atrophy over time in early-onset Alzheimer's disease: longitudinal MRI study
- Multicenter standardized 18F-FDG PET diagnosis of mild cognitive impairment, Alzheimer's disease, and other dementias
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 →