Epigenetic control of enhancers alters neuronal functions and may be involved in Alzheimer's disease (AD). 2 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Epigenetic control of enhancers alters neuronal functions and may be involved in Alzheimer's disease (AD). 2 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease (AD). 2 key findings →
Participants: 117 Evidence: low
Full summary, score breakdown and related studies → Original source
The role of DNA cytosine methylation, an epigenetic regulator of chromatin structure and function, during normal and pathological brain development and aging remains unclear. 1 key finding →
Participants: 125 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Transcriptomics and polygenic risk analysis position resilience as an intermediate AD state. 5 key findings →
Participants: 631 Evidence: low
Full summary, score breakdown and related studies → Original source
Dysregulation of sphingomyelin and ceramide metabolism have been implicated in Alzheimer's disease. 1 key finding →
Participants: 1,576 Evidence: low
Full summary, score breakdown and related studies → Original source
Understanding the tissue-specific genetic controls of protein levels is essential to uncover mechanisms of post-transcriptional gene regulation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
PS2V levels increased in AD postmortem brain but PS2V was also present at significant levels in FTD and LBD brains. 4 key findings →
Participants: 160 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
There was no difference in age acceleration between dementia cases and controls. 3 key findings →
Participants: 160 Evidence: low
Full summary, score breakdown and related studies → Original source
An overview of miRNAs altered in Alzheimer's disease (AD) was established by profiling the hippocampus of a cohort of 41 late-onset AD (LOAD) patients and 23 controls, showing deregulation of 35 miRNAs. 1 key finding →
Participants: 49 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genome-wide association studies of neurological diseases have identified thousands of variants associated with disease phenotypes. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is an urgent need to develop molecular biomarkers of brain age in order to advance our understanding of age related neurodegeneration. 3 key findings →
Participants: 700 Evidence: low
Full summary, score breakdown and related studies → Original source
The neocortex is disproportionately expanded in human compared with mouse 1,2 , both in its total volume relative to subcortical structures and in the proportion occupied by supragranular layers composed of neurons that selectively make connections within the neocortex and with other telencephalic structures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This transcriptomic network analysis of 19 brain regions provides a comprehensive assessment of the critical molecular pathways associated with AD pathology and offers new insights into molecular mechanisms underlying selective regional vulnerability to AD at different stages of the progression of cognitive compromise and development of the canonical neuropathological lesions of AD. 5 key findings →
Participants: 125 Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with Alzheimer's disease (AD) and Parkinson's disease (PD) often have overlap in clinical presentation and brain neuropathology suggesting that these two diseases share common underlying mechanisms. 1 key finding →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes are crucial to brain homeostasis, yet their changes along the spatiotemporal progression of Alzheimer's disease (AD) neuropathology remain unexplored. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are central mediators of neuroinflammation in Alzheimer's disease (AD), yet conserved microglial states and activation trajectories across AD mouse models remain incompletely defined. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia and cognitive disorders are major aging-associated pathologies. 4 key findings →
Participants: 68 Evidence: low
Full summary, score breakdown and related studies → Original source
Major depressive disorder (MDD) is linked to a higher risk of premature aging, but the mechanisms underlying this association remain unclear. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia with advancing age as its strongest risk factor. 3 key findings →
Participants: 47 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is an incurable neurodegenerative disorder in which neuroinflammation has a critical function 1 . 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The biological processes that are disrupted in the Alzheimer's disease (AD) brain remain incompletely understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer's disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the selective vulnerability of specific neuronal populations, the molecular signatures of which are largely unknown. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
9 of the 274 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.
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →