27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Single cell RNA sequencing has opened a window into clarifying the complex underpinnings of disease, particularly in quantifying the relevance of tissue- and cell-type-specific gene expression. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although human cerebellum is known to be neuropathologically impaired in Alzheimer's disease (AD) and AD-related dementias (ADRD), the cell type-specific transcriptional and epigenomic changes that contribute to this pathology are not well understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Spatial biology technologies enable high-dimensional profiling within intact tissues, revealing how molecular and cellular organization drives function and disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The complexity of Alzheimer's disease (AD) manifests in diverse clinical phenotypes, including cognitive impairment and neuropsychiatric symptoms (NPSs). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Single-nucleus transcriptomic studies have revealed glial cell states associated with Alzheimer's disease; however, these nuclei are dissociated from the complex architecture of the human neocortex. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common neurodegenerative disorder, yet the molecular mechanisms underlying its region- and cell-type-specific pathogenesis remain poorly defined. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration (FTLD), predominantly comprised of tau and TDP-43 proteinopathies, is a common cause of early-onset dementia. 3 key findings →
Participants: 566 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) contains brain derived proteins that can be leveraged as biomarkers for Alzheimer’s disease (AD) and other neurodegenerative diseases. 5 key findings →
Participants: 48 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) develops over decades, but biological processes underlying susceptibility during midlife remain poorly understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
How amyloid-β (Aβ) plaques and tau phosphorylation spatially relate to cell response and genetic variation in Alzheimer’s disease (AD) brain is currently unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current Alzheimer’s disease (AD) neuropathological metrics, including Thal phasing, and Braak staging, often do not accurately predict cognitive status: many cognitively resilient individuals have substantial pathological burdens, whereas some patients with dementia show minimal classical AD pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Structured metabolic genetic axes reveal selective and biologically distinct links between circulating metabolism and neurodegenerative disease, providing a framework for mechanism-focused follow-up beyond single-metabolite association. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies have identified nearly 100 genetic loci that affect Alzheimer’s disease risk. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the present analysis, genetic risk and end-stage AD pathology are largely decoupled at the level of individual genes and pathways but converge on a shared, pharmacologically modifiable response landscape. 1 key finding →
Participants: 3,202 Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic studies have identified thousands of variants associated with brain-related traits. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nuclear depletion of TDP-43 is a defining pathological feature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), leading to widespread RNA misprocessing, including the formation of cryptic exons. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified many loci that contribute to the risk of neurodegenerative diseases. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Single-cell RNA sequencing (scRNA-seq) studies of Alzheimer’s disease (AD) mouse models have proliferated across independent laboratories, brain regions, and platforms, yet the cross-study reproducibility of transcriptional signatures derived from such data remains underexplored. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This work suggests that although parity history and PSEN2 deficiency exert individual differing age-related effects on cognition and neurobiology, they do not act synergistically. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Endolysosomal dysfunction is a central feature of many neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings identify conserved regulatory networks that may contribute to female-biased microglial responses to AD pathology across mice and humans. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Based on the exacerbated AD pathological features and transcriptomic alterations observed in Arf4 knockdown animals, ARF4 appears to play a critical role in AD resilience and may represent a potential prognostic factor worthy of further investigation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial Alzheimer’s disease (fAD) is an early-onset form of AD caused by autosomal-dominant variants in APP, PSEN1, or PSEN2, with PSEN1 accounting for most genetically defined cases [1]. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Active PTB was associated with widespread transcriptional remodeling, with 1,389 dysregulated genes organized into 16 PTB-associated co-expression modules. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Multi-subject spatial transcriptomics is increasingly used to identify molecular differences across individuals and conditions while resolving where in tissue those differences occur. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 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 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 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 →