Genetic evidence strongly supports the view that Abeta amyloid production is central to the cause of Alzheimer's disease.
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28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Genetic evidence strongly supports the view that Abeta amyloid production is central to the cause of Alzheimer's disease.
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In all 6 patients (3 women and 3 men; mean age 61.8 years), the underlying clinical phenotype was associated with the regional distribution of the [18F]AV-1451 signal. 4 key findings →
Evidence: low
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Neurofilament light chain (NfL) is a promising biomarker for risk stratification and disease monitoring of dementia, but its utility in the preclinical disease stage remains uncertain. 4 key findings →
Participants: 975 Evidence: low
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The apolipoprotein E4 (APOE4) allele is associated with an increased risk of Alzheimer disease and a decreased risk of glaucoma, but the underlying mechanisms remain poorly understood. 3 key findings →
Evidence: low
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We provide evidence that 2 common variants within the TREM locus are associated with pathological features of AD and aging-related cognitive decline. 5 key findings →
Participants: 3,421 Evidence: low
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Dementia and gait impairments often coexist in older adults and patients with neurodegenerative disease. 1 key finding →
Evidence: low
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Alzheimer's disease (AD) care requires timely diagnosis and multidisciplinary management. 5 key findings →
Evidence: low
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Neurogenic orthostatic hypotension (nOH) is common in patients with neurodegenerative disorders such as Parkinson's disease, multiple system atrophy, pure autonomic failure, dementia with Lewy bodies, and peripheral neuropathies including amyloid or diabetic neuropathy. 5 key findings →
Evidence: low
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Heart failure is a risk factor for Alzheimer's disease and cerebrovascular disease. 5 key findings →
Design: cross-sectional Evidence: moderate
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These findings suggest that at current expected prices, neither aducanumab nor donanemab would be cost-effective for early AD in the US. 2 key findings →
Design: clinical trial Evidence: low
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The number of patients surviving with congenital heart disease (CHD) has soared over the last 3 decades. 1 key finding →
Evidence: low
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Patients with AD and patients with FTD show different disturbances in their rhythms of activity and temperature compared with each other and with normal elderly patients. 3 key findings →
Participants: 23 Evidence: moderate
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In the field of neurodegeneration, speech and language assessments are useful for diagnosing aphasic syndromes and for characterizing other disorders. 1 key finding →
Evidence: low
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Aging is a major risk factor for both genetic and sporadic neurodegenerative disorders. 5 key findings →
Evidence: low
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Neuropsychiatric symptoms (NPSs) are hallmarks of Alzheimer's disease (AD), causing substantial distress for both people with dementia and their caregivers, and contributing to early institutionalization. 5 key findings →
Evidence: low
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The Electrophysiology Professional Interest Area (EPIA) and Global Brain Consortium endorsed recommendations on candidate electroencephalography (EEG) measures for Alzheimer's disease (AD) clinical trials. 3 key findings →
Evidence: low
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The choroid plexus (ChP) is a major source of cerebrospinal fluid (CSF) production, with a direct and indirect role in protein clearance, and pathogenesis of Alzheimer's disease (AD). 3 key findings →
Participants: 509 Evidence: low
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Sex differences in Alzheimer's disease (AD) biology and progression are not yet fully characterized. 2 key findings →
Evidence: low
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Pathological hallmarks of Alzheimer's disease (AD) are deposits of amyloid beta (Aβ) and hyper-phosphorylated tau aggregates in brain plaques. 4 key findings →
Participants: 13 Evidence: low
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Missense mutations in the presenilin 1 (PS1) gene cause the most common form of dominant early-onset familial Alzheimer's disease (FAD) and are associated with increased levels of amyloid beta-peptides (A beta) ending at residue 42 (A beta 42) in plasma and skin fibroblast media of gene carriers. 4 key findings →
Evidence: low
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Neurodegenerative diseases of the central nervous system progressively rob patients of their memory, motor function, and ability to perform daily tasks. 4 key findings →
Evidence: low
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The aim of this study was to provide an update on the role of the innate immune system and neuroinflammation in the pathogenesis of Alzheimer's disease, with an emphasis on microglial receptors CD33 and TREM2. 4 key findings →
Evidence: low
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Older persons with hip fractures remain at increased risk of subsequent hip fractures. 4 key findings →
Participants: 481 Evidence: low
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Age-related hearing loss (ARHL) has been considered as a promising modifiable risk factor for cognitive impairment and dementia. 4 key findings →
Design: cross-sectional Evidence: moderate
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Within the prospective population-based Rotterdam Study, we studied lifetime risk of dementia, stroke and parkinsonism between 1990 and 2016. 4 key findings →
Participants: 102 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 →