Aging brain

About: Aging brain is a research topic. Over the lifetime, 1255 publications have been published within this topic receiving 66405 citations.

Free sterols in senile human brain.

Abstract: Autopsy material of 18 patients, who died between 66-86 years of age and of 4 ones, who died between 20 and 38 years of age was investigated. The white matter of frontal lobe, corpus callosum and cerebellum was studied using histological and biochemical methods. According to the results of neuropathological studies, the material of aged patients was divided into two subgroups: patients with vascular changes only and brains with senile atrophy of Alzheimer type. Chemical changes in all aging brain regions studied included higher proportion of desmosterol and differences in the pattern of cholesterol isomers. These findings are interpreted as suggesting some chemical transformations of cellular membranes in the cerebral white matter of the aging. The above mentioned changes were almost identical despite presence of the signs of Alzheimer's type senile atrophy, therefore it is not possible to explain their significance in developing of dementia process.

Expression of a Constitutively Active Human Insulin Receptor in Hippocampal Neurons Does Not Alter VGCC Currents.

Abstract: Memory and cognitive decline are the product of numerous physiological changes within the aging brain. Multiple theories have focused on the oxidative, calcium, cholinergic, vascular, and inflammation hypotheses of brain aging, with recent evidence suggesting that reductions in insulin signaling may also contribute. Specifically, a reduction in insulin receptor density and mRNA levels has been implicated, however, overcoming these changes remains a challenge. While increasing insulin receptor occupation has been successful in offsetting cognitive decline, alternative molecular approaches should be considered as they could bypass the need for brain insulin delivery. Moreover, this approach may be favorable to test the impact of continued insulin receptor signaling on neuronal function. Here we used hippocampal cultures infected with lentivirus with or without IRβ, a constitutively active, truncated form of the human insulin receptor, to characterize the impact continued insulin receptor signaling on voltage-gated calcium channels. Infected cultures were harvested between DIV 13 and 17 (48 h after infection) for Western blot analysis on pAKT and AKT. These results were complemented with whole-cell patch-clamp recordings of individual pyramidal neurons starting 96 h post-infection. Results indicate that while a significant increase in neuronal pAKT/AKT ratio was seen at the time point tested, effects on voltage-gated calcium channels were not detected. These results suggest that there is a significant difference between constitutively active insulin receptors and the actions of insulin on an intact receptor, highlighting potential alternate mechanisms of neuronal insulin resistance and mode of activation.