27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
It has been well established that neuronal loss within the cholinergic nucleus basalis of Meynert (nbM) correlates with cognitive decline in dementing disorders such as Alzheimer's disease (AD). 2 key findings →
Evidence: low
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Baseline data of 423 PD patients and 196 HCs yielded no between-group differences in demographic characteristics. 3 key findings →
Evidence: moderate
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Key points • Decreasing CBF relates to more advanced AD stages in all supratentorial regions. • The reduction of CBF does not reach a bottom level. • ASL-CBF has potential as a measure for disease progression in AD. 1 key finding →
Participants: 177 Evidence: moderate
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Microglia contribute to development, homeostasis, and immunity of the CNS. 4 key findings →
Evidence: low
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Microglia are phagocytic cells that survey the brain and perform neuroprotective functions in response to tissue damage, but their activating receptors are largely unknown. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Caregivers play a major role in the care of patients with dementia and are themselves at higher risk of disease. 4 key findings →
Participants: 548 Evidence: low
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Diagnoses of dementia, probable AD, and MCI in 636 autopsied subjects from the Religious Order Study and the Rush Memory and Aging Project were based on clinical evaluation and cognitive performance tests. 4 key findings →
Evidence: low
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Florbetaben PET shows high sensitivity and specificity for the detection of histopathology-confirmed neuritic β-amyloid plaques and may thus be a valuable adjunct to clinical diagnosis, particularly for the exclusion of AD.
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Huntington's disease is a neurodegenerative disorder caused by an abnormal CAG repeat expansion within exon 1 of the huntingtin gene HTT. 4 key findings →
Participants: 16 Evidence: moderate
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Delirium affected a fifth of acute medical admissions and a third of those aged ≥75 years, and was associated with increased mortality, institutionalisation and dependency, but not with increased risk of re-admission on follow-up. 4 key findings →
Participants: 308 Evidence: low
Full summary, score breakdown and related studies → Original source
People continue to receive disease-focused therapies at the end of life rather than therapies exclusively for palliation of symptoms, suggesting that treatments may vary according to the person's primary diagnosis. 2 key findings →
Design: cross-sectional Participants: 2,623 Evidence: low
Full summary, score breakdown and related studies → Original source
ECT-induced neuroplasticity in the hippocampus and amygdala relates to improved clinical response and is pronounced in regions with prominent connections to ventromedial prefrontal cortex and other limbic structures. 2 key findings →
Design: cross-sectional Participants: 43 Evidence: moderate
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[(18)F]flutemetamol amyloid PET detects primarily advanced stages of Aβ pathology in preclinical and symptomatic AD cases. 1 key finding →
Design: clinical trial Participants: 68 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genome-wide polygenic scores (GPS), which aggregate the effects of thousands of DNA variants from genome-wide association studies (GWAS), have the potential to make genetic predictions for individuals. 1 key finding →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-PET-based CSF Aβ42 cutpoints were higher and tended to reduce intercenter variability compared with clinical-based cutpoints. 3 key findings →
Participants: 433 Evidence: moderate
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The impact of inflammation suppressor pathways on Alzheimer's disease (AD) evolution remains poorly understood. 2 key findings →
Evidence: low
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The objective of this study was to compare the effect of multisensory stimulation environment (MSSE) and one-to-one activity sessions in the symptomatology of elderly individuals with severe dementia. 2 key findings →
Evidence: low
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Key experiments using fibril-free AβO solutions demonstrated that while Aβ is essential for memory loss, the fibrillar Aβ in amyloid deposits is not the agent. 2 key findings →
Evidence: low
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This human study is based on an established cohort of "SuperAgers," 80+-year-old individuals with episodic memory function at a level equal to, or better than, individuals 20-30 years younger. 4 key findings →
Participants: 21 Evidence: moderate
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Health care aides frequently report care that is rushed and tasks omitted due to lack of time. 4 key findings →
Design: cross-sectional Participants: 583 Evidence: low
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Type 2 diabetes (T2DM), Alzheimer's disease (AD), and insulin resistance are age-related conditions and increased prevalence is of public concern. 1 key finding →
Evidence: low
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TBI patients' brains were estimated to be older than their chronological age. 3 key findings →
Evidence: low
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Even without subjective cognitive complaints, higher risk of cognitive impairment is presented in the prefrail and frail individuals. 5 key findings →
Design: cross-sectional Participants: 1,686 Evidence: moderate
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Down syndrome, which arises in individuals carrying an extra copy of chromosome 21, is associated with a greatly increased risk of early-onset Alzheimer disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Diabetes mellitus is associated with an increase in the risk of dementia and the proportion of patients who convert from mild cognitive impairment (MCI) to dementia. 2 key findings →
Evidence: low
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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 records (3.7% 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 →