Midlife Chronological and Endocrinological Transitions in Brain Metabolism: System Biology Basis for Increased Alzheimer’s Risk in Female Brain
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Midlife Chronological and Endocrinological Transitions in Brain Metabolism: System Biology Basis for Increased Alzheimer’s Risk in Female Brain
The decline in brain glucose metabolism is a hallmark of late-onset Alzheimer’s disease (LOAD). a comprehensive understanding of the aging process dynamic metabolism in the brain may provide insights into the window of opportunity to promote healthy brain aging. chronological aging and endocrinological associated with glucose hypometabolism in the brain and the female brain mitochondrial adaptation.
Using a mouse model of recapitulation fundamental feature of human menopausal transition, the results of transcriptomic analysis revealed a specific phase shift in bioenergy systems biology juxtaposed with bioenergy dysregulation of brain aging in midlife women. transcriptomic profile is predictive of the results of unbiased, metabolomics and lipidomic discovery-based analysis, which revealed the dynamic adaptation of the aging of the female brain glucose utilization centric additional fuel source including amino acids, fatty acids, lipid and ketone bodies. Coupling between the brain and the peripheral metabolism system is dynamic and shifting from uncoupled to coupled under metabolic stress. Collectively, these data provide a detailed profile of the whole system transcriptomic and metabolomics underlying bioenergetic function in the brain and its relationship with metabolic response of peripheral.
Mechanically, this data provides insight into the complex dynamics and endocrinological chronological aging of bioenergy in the female brain. Translationally, findings are predictive of initiation prodromal / LOAD preclinical phase for women in middle age and highlights the therapeutic window opportunity to reduce the risk of late-onset Alzheimer’s disease. appropriate regulation and storage of cellular lipid oxidation is indispensable for the maintenance of cellular energy homeostasis and health. Mitochondrial function has proven to be a major determinant of functional lipid storage and oxidation, which is of particular interest to the adipose tissue, because it is the primary site of storage triacylglyceride in lipid droplets (LDs).
Midlife Chronological and Endocrinological Transitions in Brain Metabolism: System Biology Basis for Increased Alzheimer’s Risk in Female Brain
Dependent mitochondrial uncoupling protein signaling in plant bioenergetics and stress response
Biological function of mitochondrial uncoupling protein crops (pUCPs) has been a matter of considerable controversy. For example, PUCP capacity to uncouple respiration from ATP synthesis in vivo was never fully recognized, in contrast to the role of mammalian UCP1 (mUCP1) in uncoupling of respiration-mediated thermogenesis.
Interestingly, both pUCPs and mUCPs has been associated with the stress response and metabolic disorders. Some of the central questions that remain are how pUCPs and mUCPs comparing the biochemical, molecular and cell biology structure under physiological conditions and metabolic disturbed. This review took advantage of the large amount of data available for mUCPs to review the biochemical properties, 3D structural model and the physiological role pUCPs potential for crop development and response to stress. Biochemical properties and structure pUCPs reviewed in light of recent findings that pUCPs catalyze metabolite transport across the inner mitochondrial membrane and mUCP2 protein structures solved.
In addition, regulatory and transcriptional co-expression network UCP orthologues across species analyzed, taking advantage of publicly available datasets curated experimental. Taking these together, the biological role pUCPs analyzed in the context of their potential role in thermogenesis, ROS production, cell signaling and the regulation of cellular bioenergetics plants. Finally, pUCPs biological functions discussed in the context of their potential role in protecting against environmental stress.
