Aging brain

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

The aging brain: is function dependent on growth hormone/insulin-like growth factor-1 signaling?

Abstract: The role of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) in normal brain function is not well understood. Studies looking at cognition in humans with GH deficiency have produced controversial results. Experiments in which GH is administered to rodents have shown an apparent improvement in learning and memory. However, studies in which GH deficient or resistant mice were tested in learning and memory tasks reveal that these animals have normal cognitive performance and that their neural function does not deteriorate with age at the same rate as their normal siblings. Further research into this phenomenon revealed that these animals have elevated GH and IGF-1 expression in the hippocampus compared to normal animals. Additional studies with GH deficient and resistant mice suggested that these mutants experience a delay in age-related decline in locomotor activity and exploratory behavior. Data indicate that GH/IGF-1 deficiency and resistance do not impair neural function and instead may offer some degree of protection that results in delayed cognitive and motor aging.

Normal Aging Induces Changes in the Brain and Neurodegeneration Progress: Review of the Structural, Biochemical, Metabolic, Cellular, and Molecular Changes

Abstract: Aging is accompanied by many changes in brain and contributes to progressive cognitive decline. In contrast to pathological changes in brain, normal aging brain changes have relatively mild but important changes in structural, biochemical and molecular level. Representatively, aging associated brain changes include atrophy of tissues, alteration in neurotransmitters and damage accumulation in cellular environment. These effects have causative link with age associated changes which ultimately results in cognitive decline. Although several evidences were found in normal aging changes of brain, it is not clearly integrated. Figuring out aging related changes in brain is important as aging is the process that everyone goes through, and comprehensive understanding may help to progress further studies. This review clarifies normal aging brain changes in an asymptotic and comprehensive manner, from a gross level to a microscopic and molecular level, and discusses potential approaches to seek the changes with cognitive decline.

Altered Response Dynamics and Increased Population Correlation to Tonal Stimuli Embedded in Noise in Aging Auditory Cortex.

Abstract: Age-related hearing loss (presbycusis) is a chronic health condition that affects one-third of the world population. One hallmark of presbycusis is a difficulty hearing in noisy environments. Presbycusis can be separated into two components: alterations of peripheral mechanotransduction of sound in the cochlea and central alterations of auditory processing areas of the brain. Although the effects of the aging cochlea in hearing loss have been well studied, the role of the aging brain in hearing loss is less well understood. Therefore, to examine how age-related central processing changes affect hearing in noisy environments, we used a mouse model (Thy1-GCaMP6s X CBA) that has excellent peripheral hearing in old age. We used in vivo two-photon Ca2+ imaging to measure the responses of neuronal populations in auditory cortex (ACtx) of adult (2–6 months, nine male, six female, 4180 neurons) and aging mice (15–17 months, six male, three female, 1055 neurons) while listening to tones in noisy backgrounds. We found that ACtx neurons in aging mice showed larger responses to tones and have less suppressed responses consistent with reduced inhibition. Aging neurons also showed less sensitivity to temporal changes. Population analysis showed that neurons in aging mice showed higher pairwise activity correlations and showed a reduced diversity in responses to sound stimuli. Using neural decoding techniques, we show a loss of information in neuronal populations in the aging brain. Thus, aging not only affects the responses of single neurons but also affects how these neurons jointly represent stimuli. SIGNIFICANCE STATEMENT Aging results in hearing deficits particularly under challenging listening conditions. We show that auditory cortex contains distinct subpopulations of excitatory neurons that preferentially encode different stimulus features and that aging selectively reduces certain subpopulations. We also show that aging increases correlated activity between neurons and thereby reduces the response diversity in auditory cortex. The loss of population response diversity leads to a decrease of stimulus information and deficits in sound encoding, especially in noisy backgrounds. Future work determining the identities of circuits affected by aging could provide new targets for therapeutic strategies.