27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
EA ameliorated cognitive impairment in APP/PS1 mice by enhancing TREM2⁺ microglia-mediated Aβ clearance and suppressing neuroinflammation. scRNA-seq further revealed that EA reshaped microglial transcriptional states and intercellular communication networks in a TREM2-dependent manner. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nasu-Hakola disease (NHD), a dementia with about 200 cases worldwide, is caused by loss-of-function mutation of TYROBP , encoding DAP12, or its receptor TREM2 . 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
These data further support the use of the LOAD2.Mthfr 677C>T mouse model to study aspects of ADRD such as cerebrovascular compromise. 2 key findings →
Evidence: low
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
Microglia are key drivers of Alzheimer’s disease (AD), and TREM2, one of the strongest genetic risk factors, enables the disease-associated microglia (DAM) state required for plaque engagement. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These results suggest that the cognitive-enhancing effects of Sob-AM2 are not the result of reduced overall plaque burden. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies (DLB) is characterized by marked biological heterogeneity, only partly explained by the frequent presence of Alzheimer’s disease (AD) copathology. 4 key findings →
Design: longitudinal study Participants: 129 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
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
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
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
Butyrate, a 4-carbon fatty acid produced from insoluble starch by the gut microbiome, plays key roles in mitochondrial respiration, activation of cell-surface G-protein-coupled receptors, and protein acetylation by inhibiting histone deacetylases (HDACs). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease pathology and cognitive outcomes frequently diverge, yet current single-axis definitions cannot identify resilient (high pathology, preserved cognition) and resistant (high risk, low pathology) subgroups reliably at scale, obscuring the mechanisms that uncouple pathological burden from cognitive decline. 2 key findings →
Participants: 1,009 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genetic risks were primarily associated with Aβ and tau pathology, clinical risks with neurodegeneration, and SDoH risks with cognition, suggesting that risk factors exert differential effects on AD pathophysiology. 5 key findings →
Design: cohort study Participants: 2,276 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this cohort, APOE ε4 carrier status was related to disease severity at baseline rather than to the rate of cognitive decline over 80 weeks. 3 key findings →
Design: clinical trial Participants: 370 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Anti-amyloid antibodies represent the first disease modifying therapeutics for Alzheimers disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Haploinsufficiency of progranulin (resulting from mutations in the GRN gene) is a major genetic cause of frontotemporal dementia (FTD), which is characterized by profound changes in personality and behavior, progressive impairments in executive function, speech, language and/or movement, TDP-43 pathology, lysosomal dysfunction, and neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Individuals who carry two copies of the apolipoprotein E ε4 ( APOE ε4) allele are at high risk of developing Alzheimer’s disease (AD), yet the effects of APOE ε4 homozygosity on biological pathways related to AD over the lifespan are unknown. 1 key finding →
Participants: 413 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings implicate significant liver–brain crosstalk through which chronic alcohol exposure may modulate AD-relevant pathology and reinforce the growing recognition of the liver as a critical organ in AD pathogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases are a major threat to older adults and represent a growing global health burden as the elderly population continues to expand. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
IKZF1 is prioritised as a candidate late-disease microglial TF, supported by six convergent evidence dimensions including independent bulk replication. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 →