30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Lipid-processing microglia are among the microglial states most strongly associated with Alzheimer’s disease (AD) pathology, yet whether this association reproduces across independent cohorts, what transcriptional programs define the state, and which upstream signals and small molecules can modulate it remain unsolved. 3 key findings →
Participants: 150 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among 2711 decedents (mean [SD] age, 73.4 [14.4] years; range, 23 to 111 years; 1340 [49.4%] female), 531 (19.6%) met both thresholds, 270 (10.0%) the amyloid threshold only, 207 (7.6%) the tau threshold only, and 1703 (62.8%) neither. 3 key findings →
Design: cross-sectional Participants: 1,467 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Biological definitions of neuronal α-synuclein disease are advancing diagnosis beyond traditional clinical syndromes, but the trajectories preceding dementia and the influence of concomitant Alzheimer pathology remain uncertain. 3 key findings →
Design: longitudinal study Participants: 1,543 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Many biological quantities in omics are inherently periodic or directional, including circadian phase, cell-cycle position, and cellular orientation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sleep disturbance in Alzheimer’s disease (AD), particularly the reduction of slow wave sleep (SWS), has been proposed as a novel therapeutic target, with disease-modifying potential. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is characterised by progressive accumulation of misfolded proteins and failure of cellular clearance pathways, particularly the autophagy–lysosomal system. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Our findings indicate that HFOs likely arise from different neuronal populations and are generated through distinct mechanisms in these two models. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injuries (TBIs) are associated with increased risk of neurodegenerative disease, including Alzheimer’s disease (AD); however, the mechanisms by which TBI promotes AD pathogenesis remain poorly understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sleep disruption is common in Alzheimer’s disease (AD). 1 key finding →
Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
DORA-22 and MK-1064 rescued tauopathy-related sleep loss, and reduced agitation-like locomotion and stress-induced hyperthermic responses. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Age-related hearing loss (ARHL) is a main acquired risk factor for dementia, including Alzheimer disease (AD), but links are unknown. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Postmitotic neurons must preserve genome integrity for decades despite continuous oxidative, transcription-associated, and environmental DNA damage. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia is a progressive syndrome characterized by neurodegeneration across distributed brain networks that results in cognitive, behavioral, and functional declines. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anxiety localizes to a brain circuit resembling the AD-related atrophy network, is consistent across the AD continuum and may extend beyond AD. 5 key findings →
Design: longitudinal study Participants: 1,775 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Late-life depression (LLD) is increasingly recognized as a complex multisystem disorder associated with accelerated biological aging, impaired physiological resilience, frailty, and an increased risk of cognitive decline and dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We tested whether, across sexes, alignment with female-typical, rather than male-typical, patterns of neural functional connectivity (FC) would relate to a diagnosis (adolescent sample) or severity of symptoms (adult sample) associated with internalizing disorders, which tend to be more often diagnosed in females. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
A key pathophysiological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is loss of nuclear localization and abnormal cytoplasmic aggregation of TAR DNA-binding protein 43 (TDP-43). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Transactive response DNA-binding protein 43 (TDP-43) aggregation and loss of function are hallmark features of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) among other neurodegenerative diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders, yet the environmental drivers that accelerate its progression remain poorly defined. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Higher exposure to PM 2.5 was associated with cerebral arteriolosclerosis and atherosclerosis at death, consistent with the known vascular toxicity of this pollutant. 5 key findings →
Design: cohort study Participants: 909 Evidence: moderate
Full summary, score breakdown and related studies → Original source
However, increasing evidence indicates that systemic metabolic dysfunction, chronic inflammation, intestinal dysbiosis, hepatic abnormalities, and barrier impairment may substantially influence disease susceptibility and progression. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Metabotropic glutamate receptors (mGluRs) regulate glutamatergic transmission and have been implicated in diverse neuropsychiatric disorders, but human postmortem evidence remains fragmented. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
DMII provides a metabolomics-based framework for assessing diet-related chronic inflammation using metabolomics data. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Microglial activation and FR expression in APP/PS1 and P301S transgenic mouse models of AD was measured using flow cytometry. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglial activation and subsequent neuroinflammation involves THIK-1 (KCNK13), a Two-Pore Domain (K2P) K+ channel. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 8,460 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events