29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Chronic psychological stress is a well-known risk factor for neurodegenerative diseases including Alzheimer disease (AD), yet the underlying mechanisms remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The repeated inability of Aβ therapies to pass clinical tests in sporadic AD points to the complexity of the disease and indicates that earlier or more interventions could be necessary. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) affects over 55 million people worldwide and lacks effective disease-modifying therapies targeting neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mechanistic studies demonstrate that pharmacological modulation of microglial phenotypes inhibition of pro inflammatory mediators TNF alpha IL 1 IL 6 and targeting pathways such as NF kappa B NLRP3 inflammasome p38 MAPK JAK STAT and TREM2 can attenuate neuroinflammatory cascades and reduce amyloid beta and tau associated neurotoxicity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a neurological condition that worsens over time and is characterised by tau tangles and amyloid plaques. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dysregulated ferritinophagy-mediated ferroptosis is a pivotal AD pathogenic target. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Introdução: O sequenciamento de nova geração (NGS) tem revolucionado a compreensão da doença de Alzheimer (DA), desvendando biomarcadores genéticos e transcriptômicos que aprimoram a estrutura ATN (beta-amiloide, Tau, neurodegeneração). 5 key findings →
Evidence: low
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Alzheimer disease (AD) is a multi-factorial neurodegenerative disease that is characterized by accumulation of amyloid-beta (Aβ), protein aggregation and progressive neuronal dysfunction. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Studies in Jalisco have identified a mutation in the PSEN1 gene, associated with early-onset Alzheimer's. This variant, common in the Altos de Jalisco region, affects both men and women, causing severe symptoms such as difficulty walking and speaking. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Esse artigo buscou abordar a Doença de Alzheimer de Início Precoce (DAIP) acerca do curso clínico, dos fatores predisponentes e do manejo, por meio de uma revisão de literatura, com ênfase na diferenciação entre DAIP e Doença de Alzheimer de Início Tardio (DAIT), incluindo artigos publicados entre 2015 e 2025, obtidos nas bases de dados “Alzheimer's Association”, “ScienceDirect”, “Cochrane” e “PubMed”, utilizando as palavras-chave “Alzheimer”, “early” e “on-set”, com o conectivo AND. 4 key findings →
Evidence: low
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Sequencing revealed a biallelic SORL1 splice donor variant (c.1211 + 1G > A). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Introdução: A doença de Alzheimer (DA) é uma condição neurodegenerativa progressiva, caracterizada pelo acúmulo de placas de β-amiloide e emaranhados neurofibrilares. 5 key findings →
Evidence: low
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El objetivo de este trabajo es desarrollar un algoritmo de forrajeo de bacterias para el alineamiento múltiple de secuencias genéticas. 5 key findings →
Evidence: low
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Con el envejecimiento de la población general, el número de pacientes con epilepsia de inicio tardío crece constantemente. 5 key findings →
Evidence: low
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Este artículo cuestiona la dicotomía entre realismo y constructivismo en la filosofía de la ciencia, argumentando que resulta insuficiente para comprender entidades biomédicas como el Alzheimer. 5 key findings →
Evidence: low
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La enfermedad de Alzheimer (EA) fue descrita por primera vez en una mujer, Augusta D, cuyo caso reveló las características neuropatológicas clásicas de placas amiloides y ovillos neurofibrilares. 5 key findings →
Evidence: low
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Directed conversion of mature human cells, as from fibroblasts to neurons, is of potential clinical utility for neurological disease modeling as well as cell therapeutics. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although large numbers of microRNAs (miRNAs) expressed in Alzheimer disease (AD) have been detected, their functions and mechanisms of regulation remain to be fully clarified. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
KEY POINTSO_LIThis paper demonstrates the feasibility of implementing Geriatric ED programs with targeted support for people living with or at risk for dementia across three distinct health systems in San Francisco. 5 key findings →
Evidence: low
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ObjectivesNon-invasive brain stimulation (NIBS) holds significant promise for treating neurological and neuropsychiatric conditions, yet translation into routine clinical practice remains limited. 1 key finding →
Participants: 33 Evidence: low
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BackgroundDementia is rising worldwide, and in Alzheimer Disease (AD) the loss of communication adds to the burden. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
IntroductionGenetic studies have shown the APOL1 variant p.N264K, also called M1, is associated with markedly lower kidney disease risk when co-inherited with the G2-risk allele. 4 key findings →
Participants: 40,909 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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →