30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer disease (AD) is the neurodegenerative condition that occurs in the elderly population above 65 years old and is the major cause of dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is a multifactorial neurodegenerative disorder characterized by amyloid- β aggregation, oxidative stress, neuroinflammation, tau hyperphosphorylation, and cholinergic dysfunction. 1 key finding →
Evidence: low
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Recent progress of pharmacotherapy enabled anti-amyloid and anti-tau immunotherapy for Alzheimer disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a neurodegenerative disorder involving the amyloid-β plaque deposition, tau pathology, synaptic dysfunction, and impairment in cognition. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Progressive neurodegeneration, which causes memory loss, cognitive decline, and functional impairment is known as Alzheimer's disease, the most common type of dementia, first identified by Alois Alzheimer in 1907. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
For persons with early-stage sympathetic Alzheimer's disease (AD), including those with mild cognitive impairment and mild congitive dementia stages of the disease with confirmed amyloid pathology, KISUNLA (donanemab-azbt) is a disease-modifying treatment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Im Zuge der Alzheimerkrankheit lagern sich Beta-Amyloid-Plaques im Gehirn ab. 5 key findings →
Evidence: low
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Nößler: Selten hat die Neuanführung eines Arzneimittels so ein großes Medienecho ausgelöst wie jüngst der Markteintritt von Lecanemab und jetzt die Zulassung von Donanemab. 5 key findings →
Evidence: low
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Lecanemab ist eine Anti-Amyloid-Antikörper-Therapie, die entwickelt wurde, um toxische Amyloid-Plaques zu beseitigen und das Fortschreiten der Alzheimer-Krankheit zu verlangsamen. 4 key findings →
Evidence: low
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Introdução: Avanços recentes na pesquisa de biomarcadores e estruturas diagnósticas, como o sistema de classificação ATN, redefiniram a abordagem do diagnóstico e tratamento precoces. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ResumenLa enfermedad de Alzheimer (EA) es una enfermedad neurodegenerativa crónica que se caracteriza por la acumulación excesiva de proteína beta-amiloide y de proteína Tau fosforilada. 1 key finding →
Evidence: low
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El Alzheimer es un trastorno neurodegenerativo que afecta la cognición y memoria. 5 key findings →
Evidence: low
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Die zerebrale Amyloidangiopathie (CAA) ist eine Erkrankung, bei der sich beta-Amyloid in den Gefäßwänden des Gehirns ablagert. 5 key findings →
Evidence: low
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All articles of this category (opens in new window) Die zerebrale Amyloidangiopathie (CAA) ist eine Erkrankung, bei der sich beta-Amyloid in den Gefäßwänden des Gehirns ablagert. 5 key findings →
Evidence: low
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Wissenschaftler*innen der Washington Universität in St. Louis untersuchten in dieser aktuellen Studie Machbarkeit und Sicherheit der Therapie mit dem monoklonalen Antikörper Lecanemab bei Patientinnen und Patienten mit früher symptomatischer Alzheimer-Krankheit. 4 key findings →
Evidence: low
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Eine Möglichkeit zur Behandlung von beginnenden Alzheimer-Erkrankungen stellten Anti-Amyloid-Antikörper (AK) dar, die die Amyloidablagerungen im Gehirn reduzieren sollen. 5 key findings →
Evidence: low
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Mit der Zulassung von Lecanemab in Europa ist die Antikörpertherapie bei Alzheimer Krankheit (AD) hierzulande angekommen. 5 key findings →
Evidence: low
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Alzheimer disease is one of the causes of dementia that could make the patient lose their memories until they unable to do normal activities. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Progressive neurodegenerative disorder i.e. Alzheimer’s disease (AD) is characterized by cognitive decline, oxidative stress, and cholinergic dysfunction, β-amyloid aggregation, tau hyperphosphorylation. 5 key findings →
Evidence: low
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On June 7, 2021, the FDA granted accelerated approval to aducanumab (Aduhelm), the first new Alzheimer's drug approved since 2003 and the first ever approved for a mechanism thought to modify disease course. 3 key findings →
Design: regulatory decision Evidence: preliminary
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Elderly patients with AD hypovitaminosis D are at increased risk for hip fracture. 3 key findings →
Participants: 29 Evidence: low
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A high incidence of fractures, particularly of the hip, represents an important problem in patients with Alzheimer disease (AD), who are prone to falls and have osteoporosis. 2 key findings →
Participants: 15 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
Full summary, score breakdown and related studies → Original source Free full text
BackgroundAnti-amyloid-{beta} (A{beta}) monoclonal antibodies are disease-modifying treatments for early Alzheimers disease but are associated with amyloid-related imaging abnormalities (ARIA) and intracranial hemorrhage (ICH). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
BackgroundNon-pharmacological interventions may enhance motor-cognitive integration in prodromal Alzheimers disease (pAD). 5 key findings →
Design: randomized controlled trial Participants: 68 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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