27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
BACKGROUNDQuantitative amyloid-beta (A{beta})-PET is increasingly used in AD prevention trials. 3 key findings →
Design: longitudinal study Participants: 433 Evidence: moderate
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BackgroundPathogenic variants in GCH1 have been associated with Parkinsons disease (PD), but the clinical phenotype and longitudinal disease course of GCH1-associated PD remain incompletely characterized. 5 key findings →
Design: longitudinal study Participants: 22,825 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cognitive and behavioural impairment frequently accompanies motor decline in amyotrophic lateral sclerosis (ALS), with 15% of cases meeting the diagnostic criteria for frontotemporal dementia (FTD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Structural variants (SVs) are a major source of genetic variation yet remain underexplored in healthy aging and neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genome-wide association studies (GWAS) typically represent Alzheimers disease (AD) risk loci by a single lead SNP, although the lead SNP may capture only part of the genetic variation at a locus. 3 key findings →
Participants: 493 Evidence: low
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Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood. 1 key finding →
Evidence: low
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Genetic variation at the TMEM106B locus has been associated with Alzheimers disease (AD) and related neurodegenerative phenotypes, yet its haplotypic architecture remains incompletely resolved. 2 key findings →
Participants: 493 Evidence: low
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BackgroundAlzheimers disease (AD) is characterized by amyloid beta and tau accumulation accompanied by altered inflammatory responses. 4 key findings →
Design: cross-sectional Participants: 261 Evidence: moderate
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Hexanucleotide repeat expansions in C9orf72 are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, yet the predictive information contained within associated inflammatory and proteinopathy markers remains incompletely characterised. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundAlzheimers Disease and Related Dementias (ADRD) is a growing global public health challenge, and caregivers experience high rates of burden, unmet needs, and system failures. 1 key finding →
Evidence: low
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Alzheimers disease (AD) is defined by progressive neurodegeneration, yet a substantial fraction of its genetic risk maps to non-neuronal processes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Using the ADNI dataset, we found that the model realigned patients according to their clinical diagnoses. 1 key finding →
Design: longitudinal study Evidence: moderate
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BackgroundThe brain age gap (BAG), the difference between neuroimaging-predicted and chronological age, captures inter-individual variation in brain aging. 2 key findings →
Design: longitudinal study Participants: 202 Evidence: moderate
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KEY POINTSO_LIThis paper demonstrates the feasibility of implementing Geriatric ED programs with targeted support for people living with or at risk for dementia across three distinct health systems in San Francisco. 5 key findings →
Evidence: low
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Examples include subpopulations of CD4+ T cells associated with inflammatory bowel disease, characterized by enrichment for a multi-cytokine phenotype and overlap with the naive NF-kB-activated, central memory, and effector memory CD4+ T subtypes, and subpopulations of microglia associated with Alzheimers disease, characterized by depletion of homeostatic programs and localization to the midtemporal gyrus, dorsolateral prefrontal cortex, and medial entorhinal cortex. 3 key findings →
Evidence: low
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AbstractO_ST_ABSBackgroundC_ST_ABSGlucagon-like peptide-1 (GLP-1) receptor agonists and sodium-glucose cotransporter-2 (SGLT2) inhibitors are increasingly used for type 2 diabetes. 5 key findings →
Participants: 6,328 Evidence: low
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The feasibility criteria of >80% was met. 5 key findings →
Evidence: high
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Self-repairs - in-utterance revisions in which a speaker abandons and reformulates their speech - are a promising interpretable marker for speech-based cognitive screening. 1 key finding →
Evidence: low
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INTRODUCTIONNeurodegenerative research identifies biomarkers to confirm presence of disease and inform about risk for clinical symptoms. 4 key findings →
Evidence: low
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We examined whether their metabolomic profiles also differed and whether subtype-related metabolic patterns were associated with dementia, stroke, and all-cause mortality. 5 key findings →
Participants: 7,671 Evidence: low
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BackgroundUp to 30% of individuals harboring core Alzheimers disease (AD) neuropathology--amyloid-{beta} (A{beta};A) and tau (T)--remain cognitively unimpaired. 1 key finding →
Design: cohort study Participants: 500 Evidence: moderate
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In the fully adjusted Cox model, baseline statin exposure was associated with a lower risk of incident AMI (HR, 0.805; 95% CI, 0.731-0.887). 3 key findings →
Design: cohort study Participants: 174,014 Evidence: high
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Persistent racial disparities in dementia raise concerns regarding the validity and generalizability of existing prognostic models across diverse populations. 2 key findings →
Participants: 55,004 Evidence: moderate
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ObjectivesNon-invasive brain stimulation (NIBS) holds significant promise for treating neurological and neuropsychiatric conditions, yet translation into routine clinical practice remains limited. 1 key finding →
Participants: 33 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 →