28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Synaptic disturbances in excitatory to inhibitory (E/I) balance in forebrain circuits are thought to contribute to the progression of Alzheimer's disease (AD) and dementia, although direct evidence for such imbalance in humans is lacking. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
On NULISA, phosphorylated tau (p-tau217, p-tau231, and p-tau181), glial fibrillary acidic protein (GFAP), and microtubule-associated protein tau (MAPT-tau) showed the top significant association with amyloid beta (Aβ) positron emission tomography (PET) status, followed by the neuroinflammation markers C-C motif ligand 2 (CCL2), chitotriosidase 1 (CHIT1) and interleukin-8 (CXCL8), and the synaptic marker neurogranin (NRGN). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
There has been a rapid growth in research on peripheral fluid biomarkers for Alzheimer's disease (AD) and AD-related dementias, because they are non-invasive, relatively inexpensive and easily accessible. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Discrimination of disease-related interactions of the core subsystem and FPN was found in AD-spectrum patients, which was the neural circuit fundamental to plasma NFL disrupting cognitive integrity. 3 key findings →
Participants: 112 Evidence: low
Full summary, score breakdown and related studies → Original source
Testing an Alzheimer's disease continuum cohort, the area under the curve (AUC), sensitivity, specificity, and accuracy for the p-tau217/Aβ42 ratio reached 0.961, 93%, 92%, and 93%, respectively. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma amyloid-β (Aβ) was associated with brain Aβ deposition and Alzheimer's disease (AD) development. 4 key findings →
Participants: 449 Evidence: low
Full summary, score breakdown and related studies → Original source
The definition of Alzheimer's disease (AD) now considers the presence of the markers of amyloid (A), tau deposition (T), and neurodegeneration (N) essential for diagnosis. 2 key findings →
Participants: 172 Evidence: low
Full summary, score breakdown and related studies → Original source
The degree of PVS significantly increased with age in both, BG and CS regions independently of cardiovascular risk factors. 4 key findings →
Participants: 322 Evidence: low
Full summary, score breakdown and related studies → Original source
FUS-enhanced delivery of AAV resulted in a 12.6% knockdown of APOE ε4 gene expression in the targeted hippocampus, accompanied by an over 20% decrease in apoE4 protein levels and significant reductions in astrocyte and microglia levels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Five loci showed genome-wide significant association with CSF profiles, two were novel (rs145791381 [inflammation] and GRIN2D [synaptic functioning]) and three were previously described (APOE, TMEM106B, and CHI3L1). 5 key findings →
Participants: 205 Evidence: low
Full summary, score breakdown and related studies → Original source
The existence of human hippocampal neurogenesis has long been disputed1-12 and its relevance in cognition remains unknown. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is not an inevitable outcome of pathology but a dynamic process shaped by how brain cells respond to amyloid-β (Aβ) and tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We compared regional retention of 18F-flortaucipir between 20 patients with Lewy body disorders (LBD), 12 Alzheimer's disease patients with positive amyloid positron emission tomography (PET) scans (AD+Aβ) and 15 healthy controls with negative amyloid PET scans (HC-Aβ). 1 key finding →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The neuropathology of Parkinson's disease dementia (PDD) is heterogenous, and the impacts of each pathophysiology and their synergistic effects are not fully understood. 2 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source
Late-life depression has been consistently associated with lower gray matter volume, the origin of which remains largely unexplained. 4 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
PM2.5 can enter the central nervous system through 2 main pathways, the blood-brain barrier and olfactory neurons. 5 key findings →
Participants: 113 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) remains a widespread cause of dementia globally, and its prevalence is increasing due to the aging population. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
Nutritional supplementation is emerging as a promising strategy to support clinical management of early Alzheimer's disease (AD), partly through modulation of the intestinal microbiome via the microbiota-gut-brain axis. 1 key finding →
Participants: 22 Evidence: low
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
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 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
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
10 of the 6,970 studies in this tag that have a study page, 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 10. The same 10 appear here every time.
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
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.
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 28,580 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →