کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6804144 | 1433554 | 2015 | 51 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The perimenopausal aging transition in the female rat brain: decline in bioenergetic systems and synaptic plasticity
ترجمه فارسی عنوان
انتقال پیری انقباضی در مغز موش ماده: کاهش سیستم های بیولوژیکی و انعطاف پذیری سیناپسی
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
The perimenopause is an aging transition unique to the female that leads to reproductive senescence which can be characterized by multiple neurological symptoms. To better understand potential underlying mechanisms of neurological symptoms of perimenopause, the present study determined genomic, biochemical, brain metabolic, and electrophysiological transformations that occur during this transition using a rat model recapitulating fundamental characteristics of the human perimenopause. Gene expression analyses indicated two distinct aging programs: chronological and endocrine. A critical period emerged during the endocrine transition from regular to irregular cycling characterized by decline in bioenergetic gene expression, confirmed by deficits in fluorodeoxyglucose-positron emission tomography (FDG-PET) brain metabolism, mitochondrial function, and long-term potentiation. Bioinformatic analysis predicted insulin/insulin-like growth factor 1 and adenosine monophosphate-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1 alpha (AMPK/PGC1α) signaling pathways as upstream regulators. Onset of acyclicity was accompanied by a rise in genes required for fatty acid metabolism, inflammation, and mitochondrial function. Subsequent chronological aging resulted in decline of genes required for mitochondrial function and β-amyloid degradation. Emergence of glucose hypometabolism and impaired synaptic function in brain provide plausible mechanisms of neurological symptoms of perimenopause and may be predictive of later-life vulnerability to hypometabolic conditions such as Alzheimer's.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Aging - Volume 36, Issue 7, July 2015, Pages 2282-2295
Journal: Neurobiology of Aging - Volume 36, Issue 7, July 2015, Pages 2282-2295
نویسندگان
Fei Yin, Jia Yao, Harsh Sancheti, Tao Feng, Roberto C. Melcangi, Todd E. Morgan, Caleb E. Finch, Christian J. Pike, Wendy J. Mack, Enrique Cadenas, Roberta D. Brinton,