27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Hearing loss has been associated with cognitive decline in the elderly and is considered to be an independent risk factor for dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Severe amyloidosis and plaque-localized neuro-inflammation are key pathological features of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intracerebral injection of brain extracts containing amyloid or tau aggregates in transgenic animals can induce cerebral amyloidosis and tau pathology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau protein aggregation is a hallmark of neurodegenerative diseases, including Alzheimer's disease, making the development of anti-aggregation therapeutics a critical area of research. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Agricultural pesticide use represents one of the most geographically patterned environmental systems, yet most prior research has focused largely on individual compounds rather than correlated exposure regimes. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Informal caregivers of patients with neurodegenerative diseases are confronted with significant psychological distress. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Traditional dementia-prevention programs have limited accessibility and lack continuous monitoring, making sustained cognitive and emotional support challenging. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cleavage of the amyloid precursor protein's (APP) transmembrane domain (TMD) by γ-secretase is a crucial step in the aetiology of Alzheimer's Disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial mutations in C99 can increase the total level of the soluble Aβ peptides produced by proteolysis, as well as the Aβ42/Aβ40 ratio, both of which are linked to the progression of Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The allele ε4 of the apolipoprotein E gene (APOE ε4) is the major genetic risk factor for non-dominantly inherited Alzheimer's Disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Retention of 18F-Flortaucipir is reportedly increased in the semantic variant of primary progressive aphasia (svPPA), which is dominated by TDP-43 pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Reference region selection is important for proper amyloid PET analysis, especially in subcortical vascular dementia (SVaD) patients. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction due to the disrupting binding of amyloid beta (Aβ) and tau oligomers is one of the earliest impairments in Alzheimer's Disease (AD), driving initial cognitive deficits and clinical manifestation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The search for new therapeutic approaches to Alzheimer disease (AD) is a major goal in medicine and society, also due to the impressive economic and social costs of this disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cognitive decline in older adults has significant implications for autonomy and quality of life. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is a debilitating progressive dementia, whose pathophysiology is not fully understood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To investigate alterations in resting-state electroencephalogram (EEG) microstates across the cognitive spectrum of Parkinson's disease (PD) and to evaluate their utility as electrophysiological biomarkers of cognitive impairment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a neurodegenerative disorder, marked by senile plaques composed of amyloid-β (Aβ) peptide, neurofibrillary tangles, neuronal loss and neuroinflammation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) is a significant neurological condition characterized by progressive cognitive deterioration, with prevalence rising exponentially with age. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Multidomain lifestyle interventions can improve cognitive function and mobile health technologies can deliver cost-effective interventions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In each case the framework recovered known disease genes and identified biologically coherent, disease-specific modules: in AD, 17 stable high-confidence genes and modules enriched in lipid and cholesterol metabolism and amyloid precursor protein processing; in PD, 17 stable genes and modules associated with mitophagy, ubiquitin-proteasome signaling, and mitochondrial dysfunction; in RA, 20 stable genes and modules enriched in antigen presentation and JAK-STAT cytokine signaling. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Effect size analysis proves the fact that the hybrid model produces statistically significant performance, as well as cases of clinically meaningful improvements over lightweight CNN baselines. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →