30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Expanded hexanucleotide repeats in the chromosome 9 open reading frame 72 (C9orf72) gene are the most common genetic cause of ALS and frontotemporal degeneration (FTD). 4 key findings →
Evidence: low
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Down syndrome (DS) is a major cause of mental retardation and congenital heart disease. 2 key findings →
Evidence: low
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative diseases that overlap in their clinical presentation, pathology and genetics, and likely represent a spectrum of one underlying disease. 4 key findings →
Evidence: low
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Most inpatient users of VR described the experience as pleasant and capable of reducing pain and anxiety. 4 key findings →
Participants: 510 Evidence: moderate
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Over the past decade, a surge of evidence has documented various pathological processes in the retina of patients suffering from mild cognitive impairment, Alzheimer's disease (AD), Parkinson's disease (PD), and other neurodegenerative diseases. 1 key finding →
Design: cross-sectional Evidence: low
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Alzheimer's disease (AD) is hallmarked by amyloid plaques, neurofibrillary tangles, and widespread cortical neuronal loss (Selkoe, 2001). 4 key findings →
Evidence: low
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Among 259 945 decedents with dementia (mean [SD] age, 85.8 [8.0] years; 60.4% female), 8.3% were non-Hispanic Black, 4.4% were Hispanic, and 87.3% were non-Hispanic White. 5 key findings →
Design: cohort study Evidence: moderate
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Primary age-related tauopathy (PART) is a β-amyloid-independent tauopathy, thought by some to be a distinct process from Alzheimer disease neuropathologic change (ADNC). 3 key findings →
Design: longitudinal study Participants: 174 Evidence: moderate
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To record sleep, actigraph devices are worn on the wrist and record movements that can be used to estimate sleep parameters with specialized algorithms in computer software programs. 1 key finding →
Evidence: low
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Amyloid precursor protein (APP) proteolysis is required for production of amyloid-β (Aβ) peptides that comprise β-amyloid plaques in brains of Alzheimer's disease (AD) patients. 4 key findings →
Evidence: low
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Amyloid precursor protein (APP) proteolysis is essential for production of amyloid-β (Aβ) peptides that form β-amyloid plaques in brains of Alzheimer disease (AD) patients. 4 key findings →
Evidence: low
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Amyotrophic lateral sclerosis (ALS) is a degenerative disorder that is characterized by loss of motor neurons and shows clinical, pathological, and genetic overlap with frontotemporal dementia (FTD). 3 key findings →
Evidence: low
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Individuals living with dementia often have limited capacity to express their care preferences at the final stage of life, and therefore, are at risk of receiving end-of-life care that may not align with their preferences.1 While most people prefer to be at home in their final days of life,2 research has shown that individuals with dementia are less likely to die in a home or community setting compared to those without dementia.3, 4 Studies also suggest that the percentage of individuals with dementia who died in a home or community setting has been increasing over time.5, 6 This study sought to update the literature by examining the association between dementia status and site of death, and by comparing the trends in site of death between decedents with and without dementia using recent national data. 5 key findings →
Participants: 813,213 Evidence: low
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The neurosensory retina emerges as a prominent site of Alzheimer's disease (AD) pathology. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common progressive dementia and is pathologically characterized by brain deposition of amyloid-beta (Abeta) peptide as senile plaques. 4 key findings →
Evidence: low
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PLWD proactively enrolled in a dementia care program have high baseline rates of behavioral issues and their caregivers have elevated depression and stress scores. 2 key findings →
Design: longitudinal study Participants: 195 Evidence: moderate
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Using the RGC marker ribonucleic acid binding protein with multiple splicing (RBPMS) and Nissl staining, we found a 46–56% reduction in RBPMS + RGCs and Nissl + neurons in the ganglion cell layer (GCL) of MCI and AD retinas ( P < 0.05–0.001). 5 key findings →
Evidence: low
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The mean age of the 3 women and 18 men was 50 years (range, 26-68 years). 5 key findings →
Evidence: low
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The Alzheimer amyloid protein precursor (APP) has previously been localized to human chromosome 21q11.2-q21. 1 key finding →
Evidence: low
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We enrolled 195 patients in the CARES dementia care program. 3 key findings →
Participants: 195 Evidence: low
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Alzheimer's disease and related dementias (ADRD) affects millions of patients worldwide and is a leading cause of morbidity in older adults. 4 key findings →
Evidence: low
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The Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet has emerged as a promising dietary pattern associated with reduced Alzheimer's disease (AD) risk, supported by growing evidence that both diet and the gut microbiota are modifiable contributors to disease development and progression. 1 key finding →
Evidence: low
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Research participants enrolled in Falls Prevention EBPs reported decreased levels of loneliness and social isolation and were referred by physicians, social workers, and pharmacists using an order in the electronic medical record (EMR). 2 key findings →
Participants: 382 Evidence: low
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ImportanceThe ASPREE randomized trial found no overall benefit of low-dose aspirin for disability-free survival among older adults. 4 key findings →
Design: randomized controlled trial Evidence: high
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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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events