Parkinson's disease (PD) is a common motor disorder of mysterious etiology. 4 key findings →
Evidence: low
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28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Parkinson's disease (PD) is a common motor disorder of mysterious etiology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Being overweight or obese, as measured with body-mass index or central adiposity (waist circumference), and the trajectory of body-mass index over the life course have been associated with brain atrophy, white matter changes, disturbances of blood-brain barrier integrity, and risk of all-cause late-onset dementia and Alzheimer's disease. 4 key findings →
Evidence: low
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Triple-A syndrome (MIM 231550; also known as Allgrove syndrome) is an autosomal recessive disorder characterized by adrenocorticotropin hormone (ACTH)-resistant adrenal insufficiency, achalasia of the oesophageal cardia and alacrima. 4 key findings →
Evidence: low
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Alzheimer's Disease (AD) is a chronic neurodegenerative disorder and the most common type of dementia (60-80% of cases). 4 key findings →
Evidence: low
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The final study sample comprised 8,797 participants (53.5% women, mean age at HUNT4 77.8 [SD 6.2]). 5 key findings →
Participants: 8,797 Evidence: low
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VLAHE residents had fewer hospitalizations and shorter stays (10.5 vs 15.2 days, P = .0004) than comparable NH residents, particularly for acute care. 5 key findings →
Design: longitudinal study Evidence: moderate
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Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →
Design: case-control Evidence: high
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Genotyping of patients is useful to confirm the diagnosis in the latter patients and essential for future prenatal diagnosis. 5 key findings →
Evidence: low
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Hippocampal atrophy, as evidenced using magnetic resonance imaging (MRI), is one of the most validated, easily accessible and widely used biomarkers of Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Amyloid pathology is associated with changes in structural MRI measures in CN and MCI. 3 key findings →
Participants: 337 Evidence: low
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Cerebral ischemic small vessel disease (SVD) is the leading cause of vascular dementia and a major contributor to stroke in humans. 5 key findings →
Evidence: low
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Mild cognitive impairment (MCI) was proposed as a nosological entity referring to elderly people with mild cognitive deficit but no dementia. 1 key finding →
Evidence: low
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Atherosclerosis is driven by the expansion of cholesterol-loaded 'foamy' macrophages in the arterial intima. 4 key findings →
Evidence: low
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Differential diagnosis between dementia with Lewy bodies (DLB) and Alzheimer's disease (AD) is not straightforward, especially in the early stages of disease. 4 key findings →
Participants: 57 Evidence: low
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Current AT(N) stratification for Alzheimer's disease (AD) accounts for complex combinations of amyloid (A), tau proteinopathy (T) and neurodegeneration (N) signatures. 4 key findings →
Evidence: moderate
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Cerebral amyloid angiopathy (CAA) is currently diagnosed using MRI-based Boston criteria. 4 key findings →
Design: cohort study Participants: 102 Evidence: moderate
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The Mini-Mental State Examination (MMSE) measures global cognitive performance and is often used as a screening test for dementia. 4 key findings →
Design: cross-sectional Evidence: moderate
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Delayed neuronal loss and brain atrophy after cerebral ischemia contribute to stroke and dementia pathology, but the mechanisms are poorly understood. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) neuropathology is extremely heterogeneous, and the evolution from preclinical to mild cognitive impairment until dementia is driven by interacting genetic/biological mechanisms not fully captured by current clinical/research criteria. 2 key findings →
Participants: 20 Evidence: low
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= 0.81). NfL levels were not significantly associated with GDS-15 in a population of community-dwelling older adults without dementia. 4 key findings →
Design: cross-sectional Participants: 512 Evidence: low
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MEG 16-38Hz spectral power, particularly over parieto-occipital magnetometers, was significantly reduced in the AD progression group. 5 key findings →
Participants: 117 Evidence: low
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It has been well documented that neurotrophins, including brain-derived neurotrophic factor (BDNF), are severely affected in Alzheimer's disease (AD), but their administration faces a myriad of technical challenges. 4 key findings →
Evidence: low
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PICALM, a clathrin adaptor protein, plays important roles in clathrin-mediated endocytosis in all cell types. 4 key findings →
Evidence: low
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Our aim was to investigate the extent of white matter tissue damage in patients with early Alzheimer disease (AD) using diffusion tensor magnetic resonance imaging (DTI). 2 key findings →
Participants: 12 Evidence: low
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These data provide evidence for clinical and functional heterogeneity among subjects with aMCI and suggest that 18FDG-PET findings combined with memory scores may be useful in predicting short-term conversion to AD. 3 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →