The effect of insulin resistance on amygdale glucose metabolism alterations in experimental Alzheimer’s disease

Горина, Я. В.; Комлева, Ю К; Lopatina, Olga; Chernykh, Anatoliy I.; Салмина, А. Б.

doi:10.20538/1682-0363-2017-4-106-115

Cited by 2 publications

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References 27 publications

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“…These events lead to significant changes in neuronal metabolism like elevated glucose utilization and conversion to lactate, facilitation of mitochondrial oxidative phosphorylation (OXPHOS) [ 81 ]. Thus, it is not surprising that aberrant insulin signaling and brain glucose hypometabolism are considered as components of the pathogenesis of Alzheimer’s disease and progression of physiological aging: these metabolic phenomena trigger a cascade of pathological events, namely mitochondrial dysfunction, oxidative stress, excitotoxicity, apoptosis, and activation of pro-inflammatory cytokines [ 81 , 82 , 83 , 84 ] ( Figure 1 ). Recently, systemic insulin resistance and development of diabetes mellitus in ageing mice (P350) that underwent ELS in the form of maternal separation at the neonatal period was clearly demonstrated [ 85 ], but whether these data might be extrapolated on the cerebral mechanisms of insulin signaling remains unclear.…”

Section: Developmental Aspects Of Brain Metabolism and Effects Of Elsmentioning

confidence: 99%

Early Life Stress and Metabolic Plasticity of Brain Cells: Impact on Neurogenesis and Angiogenesis

et al. 2021

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Early life stress (ELS) causes long-lasting changes in brain plasticity induced by the exposure to stress factors acting prenatally or in the early postnatal ontogenesis due to hyperactivation of hypothalamic-pituitary-adrenal axis and sympathetic nervous system, development of neuroinflammation, aberrant neurogenesis and angiogenesis, and significant alterations in brain metabolism that lead to neurological deficits and higher susceptibility to development of brain disorders later in the life. As a key component of complex pathogenesis, ELS-mediated changes in brain metabolism associate with development of mitochondrial dysfunction, loss of appropriate mitochondria quality control and mitochondrial dynamics, deregulation of metabolic reprogramming. These mechanisms are particularly critical for maintaining the pool and development of brain cells within neurogenic and angiogenic niches. In this review, we focus on brain mitochondria and energy metabolism related to tightly coupled neurogenic and angiogenic events in healthy and ELS-affected brain, and new opportunities to develop efficient therapeutic strategies aimed to restore brain metabolism and reduce ELS-induced impairments of brain plasticity.

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