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Aging brain
About: Aging brain is a research topic. Over the lifetime, 1255 publications have been published within this topic receiving 66405 citations.
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TL;DR: It is suggested that the imbalance toward inhibition resulting from a decrease of glutamate content in the aging cerebral cortex, together with GABAergic system ineffectiveness in upregulating GABA level after sensory training, contributes to the impairment of learning-dependent cortical plasticity.
Abstract: Age-related molecular changes in the synapse can cause plasticity decline. We found an impairment of experience-dependent cortical plasticity is induced by short lasting sensory conditioning in aged mice. However, extending the training procedure from 3 to 7 days triggered plasticity in the aged cortex of the same range as in young mice. Additionally, GABAergic markers (GABA, GAD67, VGAT) in young and aged groups that showed the plastic changes were upregulated. This effect was absent in the aged group with impaired plasticity, while the expression of Vglut1 increased in all trained groups. This may reflect the inefficiency of inhibitory mechanisms in the aging brain used to control increased excitation after training and to shape proper signal to noise ratio, which is essential for appropriate stimuli processing. HPLC analysis showed that the glutamate/GABA ratio was significantly reduced in aged animals due to a significant decrease in glutamate level. We also observed a decreased expression of several presynaptic markers involved in excitatory (vesicular glutamate transporter-vglut2) and inhibitory (glutamic acid decarboxylase-GAD67, vesicular GABA transporter VGAT) transmission in the aged barrel cortex. These changes may weaken the plasticity potential of neurons and impede the experience-dependent reorganization of cortical connections. We suggest that the imbalance toward inhibition resulting from a decrease of glutamate content in the aging cerebral cortex, together with GABAergic system ineffectiveness in upregulating GABA level after sensory training, contributes to the impairment of learning-dependent cortical plasticity.
44 citations
TL;DR: Age-related decreases in alpha-synuclein were widespread throughout the mouse brain, affecting other regions (e.g., hippocampus) besides the substantia nigra, suggesting that loss of alpha- synuclein could contribute to or be a marker of synaptic dysfunction in the aging brain.
44 citations
01 Jan 1992
TL;DR: This book discusses memory, language and Decision-Making: Contributions from the Lesion Method in Humans, and the early detection of Brain Pathology in Alzheimer's Diesease.
Abstract: Introduction: Neurophilosophy and Alzheimer's Disease.- Temporal Anomalies of Consciousness: Implications of the Uncentered Brain.- Intertheoretic Reduction: A Neuroscientist's Field Guide.- Language Comprehension in Ape and Child: Evolutionary Implications.- A Cognitive Neuroscience of Alzheimer's Disease: What Can be Learned from Studies of Visual Imagery?.- Neuronal Models of Cognitive Functions Associated with the Prefrontal Cortex.- Exploring Memory in the Aging Brain from the Perspective of Recent Split Brain Studies.- Alzheimer's Disease: Disruption of Mind-Brain Relations.- Memory, Language and Decision-Making: Contributions from the Lesion Method in Humans.- The Pathogenesis of Alzheimer's Disease. What Causes Dementia?.- The Early Detection of Brain Pathology in Alzheimer's Diesease.- Consciousness: Evidence of Four Components in Alzheimer's Disease.
44 citations