As the world's population ages and people live longer, the changes in the aging brain present substantial challenges to our health and society. With greater longevity come age-related diseases, many of which have direct and indirect influences on the health of the brain. Although there is some degree of predictable decline in brain functioning with aging, meaningful cognitive decline is not inevitable and is perhaps preventable. In this review, we present the case that the course of aging-related brain disease and dysfunction can be modified. We present the evidence for conditions and risk factors that may contribute to cognitive decline and dementia and for interventions that may mitigate their impact on cognitive functioning later in life, or even prevent them and their cognitive sequelae from developing. Although much work remains to be done to meet the challenges of the aging brain, strategies to promote its health have been demonstrated and offer much promise, which can only be realized if we mount a vigorous public health effort to implement these strategies.
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http://dx.doi.org/10.1016/j.jagp.2018.12.016 | DOI Listing |
J Integr Neurosci
December 2024
Department of Human Anatomy, School of Basic Medical Sciences, Wannan Medical College, 241002 Wuhu, Anhui, China.
Background: K48-linked ubiquitin chain (Ub-K48) is a crucial ubiquitin chain implicated in protein degradation within the ubiquitin-proteasome system. However, the precise function and molecular mechanism underlying the role of Ub-K48 in the pathogenesis of Alzheimer's disease (AD) and neuronal cell abnormalities remain unclear. The objective of this study was to examine the function of K48 ubiquitination in the etiology of AD, and its associated mechanism of neuronal apoptosis.
View Article and Find Full Text PDFNetw Neurosci
December 2024
Laufer Center for Physical and Quantitative Biology, Stony Brook University, Stony Brook, NY, USA.
The integration-segregation framework is a popular first step to understand brain dynamics because it simplifies brain dynamics into two states based on global versus local signaling patterns. However, there is no consensus for how to best define the two states. Here, we map integration and segregation to order and disorder states from the Ising model in physics to calculate state probabilities, and , from functional MRI data.
View Article and Find Full Text PDFAging Brain
November 2024
School of Psychological Science, University of Western Australia, Crawley, Western Australia, Australia.
Sleep discrepancy (negative discrepancy reflects worse self-reported sleep than objective measures, such as actigraphy, and positive discrepancy the opposite) has been linked to adverse health outcomes. This study is first to investigate the relationship between sleep discrepancy and brain glucose metabolism (assessed globally and regionally via positron emission tomography), and to evaluate the contribution of insomnia severity and depressive symptoms to any associations. Using data from cognitively unimpaired community-dwelling older adults ( = 68), cluster analysis was used to characterise sleep discrepancy (for total sleep time (TST), wake after sleep onset (WASO), and sleep efficiency (SE)), and logistic regression was used to explore sleep discrepancy's associations with brain glucose metabolism, while controlling for insomnia severity and depressive symptoms.
View Article and Find Full Text PDFAging Brain
November 2024
International Institute for Integrative Sleep Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-0006, Japan.
J Clin Neurosci
December 2024
Faculdade de Farmácia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. Electronic address:
Alzheimer's disease (AD) is the most common cause of dementia, characterized by progressive cognitive and functional decline and is associated with aging. Chronic inflammatory processes are also involved in its the etiology, as the consequence or cause of proteinopathy (amyloid and tau load in the brain). This study aimed to investigate the complete blood count and systemic inflammation indices in 61 individuals with AD, compared to 59 cognitively healthy individuals as controls.
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