Plain Language SummaryWhat is this summary about? 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plain Language SummaryWhat is this summary about? 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Zusammenfassung Die Alzheimer Krankheit (AD) ist eine schwere und fortschreitende neurodegenerative Erkrankung des Gehirns, die bislang mit primär nur symptomatisch wirksamen medikamentösen und nicht-medikamentösen Therapieformen als Standardtherapie behandelt wird. 5 key findings →
Evidence: low
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ε4 heterozygous woman with mild cognitive impairment and CSF biomarker evidence of AD underwent treatment with intravenous lecanemab. 4 key findings →
Evidence: low
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Alzheimer's disease is the leading cause of dementia worldwide. 1 key finding →
Evidence: low
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Alzheimer’s disease (AD), the leading cause of dementia, is a multifaceted neurodegenerative disorder characterized by amyloid-beta (Aβ) aggregation, tau pathology, and neuroinflammation. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) stands as one of the primary neurological disorders affecting humans. 2 key findings →
Evidence: low
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Alzheimer disease (AD) is a most common form of dementia and eventually causes impairments of learning ability and memory function. 1 key finding →
Evidence: low
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Amnestic mild cognitive impairment (aMCI) represents a critical prodromal stage of Alzheimer's disease (AD), yet effective therapeutic interventions to prevent or delay this conversion remain an unmet clinical need. 5 key findings →
Evidence: low
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Donanemab increased total healthcare costs ($300,689 vs. $178,121) and societal costs ($389,113 vs. $283,618) compared with standard care per capita, while improving health outcomes (4.38 vs. 4.01 QALYs) per capita. 5 key findings →
Evidence: moderate
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Orally dosed D-AIP possessed favourable biostability, pharmacokinetics, and brain region distribution. 5 key findings →
Evidence: low
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Like CP2, C458 and C273 weakly inhibit mtCI, leading to AMPK activation, which triggers a neuroprotective stress response. 5 key findings →
Evidence: low
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Mild cognitive impairment (MCI) is the in-between stage between healthy cognitive aging and neurodegenerative diseases such as Alzheimer's disease (AD). 5 key findings →
Evidence: low
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Letter in response to the article by Wang et al. recently published in Alzheimer's & Dementia (Wang W, Wang Q, Qi X, Gurney M, Perry G, Volkow ND, Davis PB, Kaelber DC, Xu R. Associations of semaglutide with first-time diagnosis of Alzheimer's disease in patients with type 2 diabetes: Target trial emulation using nationwide real-world data in the US. 3 key findings →
Evidence: low
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A 52-year-old male with early-stage Alzheimer's disease and long-standing anxiety received 30 repetitive transcranial magnetic stimulation sessions over 8 months and 20-month Mediterranean diet intervention. 5 key findings →
Evidence: low
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This study offers evidence of functional and neuroprotective effects of two weeks treatment with a Ptychopetalum olacoides extract against Aβ peptide-induced neurotoxicity in mice. 1 key finding →
Evidence: low
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= 314,472) as early OAC initiation. Median age for both cohorts was 78 years. 5 key findings →
Evidence: low
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Monoclonal antibodies such as lecanemab and donanemab show reduction in amyloid plaque and slowing of cognitive and functional decline (modest) in early AD (mild cognitive impairment or mild dementia). 5 key findings →
Design: narrative review Evidence: high
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Monoclonal antibodies such as lecanemab and donanemab show reduction in amyloid plaque and slowing of cognitive and functional decline (modest) in early AD (mild cognitive impairment or mild dementia). 5 key findings →
Design: narrative review Evidence: high
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Alzheimer’s disease (AD) is characterized by progressive accumulation of amyloid-β (Aβ) peptides, initiating a pathological cascade from soluble monomers to toxic oligomers, protofibrils, fibrils, and ultimately extracellular amyloid plaques that contribute to synaptic dysfunction and neuronal degeneration. 1 key finding →
Evidence: low
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La hipótesis amiloide, que propone la acumulación del péptido ?-amiloide (?A) en la sinapsis, es el factor clave de la patogénesis de la enfermedad de Alzheimer (EA) y esta ha sido la idea dominante en el campo de la investigación de la EA durante casi 30 años. 5 key findings →
Evidence: low
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HIIT alone and in combination with CBD treatment significantly improved cognitive impairment induced by AD. 4 key findings →
Evidence: low
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Introducción: La enfermedad de Alzheimer (EA) representa la causa más común de demencia a nivel mundial, caracterizada por un deterioro progresivo de la memoria y otras funciones cognitivas. 5 key findings →
Evidence: low
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The VHA is well-positioned to use a hybrid approach-both telehealth and in-person care-to support the provision of amyloid-targeting therapies for veterans with AD. 2 key findings →
Evidence: low
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Alzheimer disease (AD) is a major health issue of global concern whereby there are minimal treatment options. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is the most common form of dementia, characterized by progressive cognitive decline, memory impairment, synaptic dysfunction, and neurodegeneration. 2 key findings →
Evidence: low
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.
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 →