28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
The Alzheimer’s disease (AD) brain is characterized by dysregulated expression of multiple microRNAs (miRNA), positioning them as promising diagnostic and therapeutic targets. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Immunoproteasome induction is prominent in Alzheimer’s disease (AD), but whether it protects proteostasis or amplifies neuroinflammation remains unresolved. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) disproportionately affects women, who exhibit greater vulnerability to Tau pathology and neuroinflammation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protein misfolding and aggregation, including amyloid fibril formation, underlie a large class of human diseases including prominent neurological disorders such as Alzheimer’s and Parkinson’s disease. 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
Familial Alzheimer’s disease (AD) mutations in amyloid precursor protein (APP) alter amyloid-β (Aβ) secretion profiles, but their effects on neuronal protein and lipid homeostasis remain incompletely understood. 4 key findings →
Design: longitudinal study Evidence: moderate
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
Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) frequently co-occurs with Alzheimer’s disease (AD) pathology and has been studied mainly in older populations. 3 key findings →
Participants: 196 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is accompanied by profound cerebrovascular dysfunction, yet it remains unclear whether endothelial abnormalities reflect only vascular injury or altered regulatory states connecting vascular remodeling with metabolic and immune function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These integrated findings support H. erinaceus as a candidate adjunct to donepezil, with possible complementary effects on amyloidogenic processing and intracellular clearance. 3 key findings →
Evidence: low
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
Traumatic brain injury (TBI) is a risk factor for Alzheimer’s disease (AD), and both conditions are associated with impaired glucose metabolism and mitochondrial dysfunction. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intracellular neurofibrillary tangles formed from hyperphosphorylated tau and extracellular amyloid plaques containing aggregated Aβ-peptides, specific cleavage products of the Amyloid Precursor Protein (APP), are the primary histopathological hallmarks of Alzheimer’s Disease (AD), the leading cause of dementia in humans. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
2µM FAM labelled β-amyloid 1–40 was transported through CLEFF4 cells with an apparent permeability (Papp) of 4.47x10 − 6 cm/sec in the efflux direction (Basolateral (Bas) to apical (Ap)) while Ap to Bas direction was only 1.67x10 − 6 cm/sec. 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
Alzheimer’s Disease (AD) is characterised by two histopathological hallmarks, intracellular tau-containing neurofibrillary tangles and extracellular amyloid plaques containing β-amyloid (Aβ), a specific cleavage product of Amyloid Precursor Protein (APP). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
MRI studies have mapped the atrophic signature that distinguishes Alzheimer's disease (AD), isolating regions differentially vulnerable to its age-dependent neurodegenerative process. 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
Although Alzheimer’s disease (AD) and glioblastoma (GBM) share common aging-related risk factors, they lead to opposite cellular fates—neurodegeneration versus uncontrolled proliferation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Single-nucleus RNA-seq (snRNA-seq) studies of Alzheimer’s disease (AD) routinely filter nuclei by mitochondrial percentage (%MT) or remove mitochondrial genes, yet whether these reads carry information about cognition is rarely examined. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sulforaphane (SFN), a natural isothiocyanate from cruciferous vegetables, exerts neuroprotective effects through mechanisms extending beyond canonical Nrf2/ARE activation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
For a long time, the protein coding potential of our genome was underestimated. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Vascular pathology is an important contributor to dementia, and astrocyte dysfunction is increasingly recognized as a key mediator of cerebrovascular injury. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 7,799 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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →