Beta amyloid is one of the major histopathological hallmarks of Alzheimer's disease.
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31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Beta amyloid is one of the major histopathological hallmarks of Alzheimer's disease.
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Prevention of Alzheimer disease (AD) is a national and global imperative. 5 key findings →
Evidence: low
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Neuritic plaques are a defining feature of Alzheimer disease (AD) pathology. 4 key findings →
Evidence: low
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Amyloid-related imaging abnormalities (ARIA) is a term introduced in 2010 to encompass a spectrum of MRI findings observed in patients receiving investigational anti-amyloid beta (Aβ) immunotherapies for Alzheimer disease (AD). 5 key findings →
Evidence: low
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Amyloid-PET quantification through the tracer-independent Centiloid (CL) scale has emerged as an essential tool for the accurate measurement of amyloid-β (Aβ) pathology in Alzheimer's disease (AD) patients. 2 key findings →
Evidence: low
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The present study indicated that most individuals with the comorbidity of epilepsy and dementia have complex partial seizures that may be adequately controlled on AED therapy. 4 key findings →
Participants: 63 Evidence: low
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Alzheimer disease (AD) is the most common form of dementia worldwide. 5 key findings →
Evidence: low
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The median PPA and NPA were 83.4% and 88.9%, respectively, with lower bounds of 2-sided 95% CIs being 50% or greater for all readers. 4 key findings →
Design: clinical trial Participants: 140 Evidence: low
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Antiamyloid antibodies have been used to reduce cerebral amyloid-beta (Aβ) load in patients with Alzheimer's disease. 5 key findings →
Evidence: low
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The advent of amyloid-β (Aβ) and tau PET imaging has revolutionized Alzheimer disease (AD) research, enabling in vivo detection of hallmark pathologies and transforming both diagnosis and therapeutic development. 5 key findings →
Evidence: low
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AD mice showed early decreases in NVC and bilateral connectivity (BC) in motor and cingulate cortex, and hypoconnectivity within the sensory-motor network. 5 key findings →
Evidence: low
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Two monoclonal antibodies (mAbs), aducanumab and lecanemab, have received accelerated approval from the US FDA for initiation of treatment in early Alzheimer's disease patients who have proven β-amyloid pathology (Aβ). 2 key findings →
Evidence: low
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There is an urgent need for novel therapeutic approaches for AD. 1 key finding →
Evidence: low
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Alzheimer disease (AD) is one of the most prevalent chronic medical conditions affecting the elderly population. 2 key findings →
Evidence: low
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In vivo imaging of fibrillar β-amyloid deposits may assist clinical diagnosis of Alzheimer's disease (AD), aid treatment selection for patients, assist clinical trials of therapeutic drugs through subject selection, and be used as an outcome measure. 5 key findings →
Evidence: low
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The current drug treatment for Alzheimer's disease (AD) is only partially and temporary effective. 1 key finding →
Evidence: low
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Tauvid has been approved by the U.S. Food and Drug Administration (FDA) in 2020 for positron emission tomography (PET) imaging of adult patients with cognitive impairments undergoing evaluation for Alzheimer's disease (AD) based on tau pathology. 5 key findings →
Evidence: low
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Hereditary diseases are caused by mutations in genes, and more than 7,000 rare diseases affect over 30 million Americans. 5 key findings →
Evidence: low
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The density of brain amyloid-beta neuritic plaque accumulation, a marker of Alzheimer's disease (AD), can be visualized and quantified using amyloid-positron emission tomography (PET). 5 key findings →
Evidence: low
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Psychotic symptoms in Parkinson's disease (PD) are relatively common and, in addition to creating a disturbance in patients' daily lives, have consistently been shown to be associated with poor outcome. 5 key findings →
Design: open-label trial Evidence: high
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Depression is one of the most frequent and burdensome non-motor symptoms in Parkinson's disease (PD), across all stages. 1 key finding →
Evidence: low
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Complex IgG autoantibody repertoires were present in all patients with glaucoma as well as healthy subjects from both the German and the United States study population. 5 key findings →
Participants: 20 Evidence: low
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Antidepressants have modest efficacy in late-life depression (LLD), perhaps because various neurobiologic processes compromise frontolimbic networks required for antidepressant response. 2 key findings →
Evidence: low
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Senolytics are a class of drugs that selectively clear senescent cells (SC). 5 key findings →
Evidence: low
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Flavonoids are a class of natural substances present in plants, fruits, vegetables, wine, bulbs, bark, stems, roots, and tea. 5 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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