[This corrects the article DOI: 10.1039/D1RA06146A.].
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http://dx.doi.org/10.1039/d1ra90163j | DOI Listing |
J Mol Evol
January 2025
Diabetes and Metabolism Research Institute, Beckman Research Institute of City of Hope, Duarte , USA.
Pituitary
January 2025
Department of Endocrinology, Diabetology & Metabolism, Faculty of Medicine, Antwerp University Hospital, Drie Eikenstraat 655, Edegem, B-2650, Belgium.
Alzheimers Dement
December 2024
Huashan Hospital, Fudan University, Shanghai, Shanghai, China.
Background: Cognition and its two critical proxies, socioeconomic status (SES) and educational attainment (EA), contribute substantially to human health and are heritable. Elucidating the genetic characteristics of SES/EA/Cognition not only helps to understand the innate individual differences in cognition, but also aids in unraveling the biological mechanisms of complex cognitive-related disorders such as Alzheimer's disease (AD). Here, we explored the rare and common protein-coding variants impacting the comprehensive cognition phenotypic spectrum by leveraging large-scale exomes.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Background: Individuals with early stages of cognitive decline face a significant stagnation in their financial capacity, leading to a decrease in quality of life. However, whether changes in brain function are associated with financial capacity remains unclear. Here, we evaluate the association between financial capacity and brain glucose metabolism.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Northwestern University, Chicago, IL, USA.
Background: Apolipoprotein E4 (E4) is the strongest genetic risk factor for sporadic Alzheimer's Disease (AD), and aging is the greatest overall risk factor for AD. Many cellular and molecular changes occur within the brain throughout aging, one of which being the increased bone morphogenetic protein 4 (BMP4) signaling. As APOE and BMPs are known to interact in non-neuronal organs, we hypothesized that enhanced BMP signaling in the brain may interact with APOE in a genotype-dependent manner to initiate or exacerbate neuropathological cascades relevant to AD.
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