Aging brain

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

Higher physiological vulnerability to hypoxic exposure with advancing age in the human brain.

Abstract: The aging brain is associated with atrophy along with functional and metabolic changes. In this study, we examined age-related changes in resting brain functions and the vulnerability of brain phys...

Plasticity Related Gene 3 (PRG3) overcomes myelin-associated growth inhibition and promotes functional recovery after spinal cord injury

Abstract: The Plasticity Related Gene family covers five, brain-specific, transmembrane proteins (PRG1-5, also termed LPPR1-5) that operate in neuronal plasticity during development, aging and brain trauma. Here we investigated the role of the PRG family on axonal and filopodia outgrowth. Comparative analysis revealed the strongest outgrowth induced by PRG3 (LPPR1). During development, PRG3 is ubiquitously located at the tip of neuronal processes and at the plasma membrane and declines with age. In utero electroporation of PRG3 induced dendritic protrusions and accelerated spine formations in cortical pyramidal neurons. The neurite growth promoting activity of PRG3 requires RasGRF1 (RasGEF1/Cdc25) mediated downstream signaling. Moreover, in axon collapse assays, PRG3-induced neurites resisted growth inhibitors such as myelin, Nogo-A (Reticulon/RTN-4), thrombin and LPA and impeded the RhoA-Rock-PIP5K induced neurite repulsion. Transgenic adult mice with constitutive PRG3 expression displayed strong axonal sprouting distal to a spinal cord lesion. Moreover, fostered PRG3 expression promoted complex motor-behavioral recovery compared to wild type controls as revealed in the Schnell swim test (SST). Thus, PRG3 emerges as a developmental RasGRF1-dependent conductor of filopodia formation and axonal growth enhancer. PRG3-induced neurites resist brain injury-associated outgrowth inhibitors and contribute to functional recovery after spinal cord lesions. Here, we provide evidence that PRG3 operates as an essential neuronal growth promoter in the nervous system. Maintaining PRG3 expression in aging brain may turn back the developmental clock for neuronal regeneration and plasticity.

Aerobic training as a means to enhance inhibition: what's yet to be studied?

Abstract: Some of the neurodegenerative processes in healthy aging, including changes in structural and biochemical properties of the brain, are argued to affect cortical inhibitory functions. Age-related deficits in the ability to control cerebral inhibition may explain wide range of motor and cognitive deficits that healthy older adults experience in daily life such as impaired coordination skills and declines in attention, concentration, and learning abilities. Importantly, evidence from many studies suggests that impaired inhibitory control in advancing age can be delayed or even alleviated by aerobic exercise training. Findings from a recent study by Duchesne and colleagues (2015) may provide insights into this process. First, observations from Duchesne et al. indicated that aerobic exercise training program improved cognitive inhibitory functioning in both patients with Parkinson’s disease (PD) and matched older controls. Second, Duchesne et al. showed that cognitive inhibition and motor skills were highly correlated both pre- and post-exercise in PD but not in controls. Based on the aforementioned findings we highlight possible mechanisms that may play a role in the interactions between cognitive and motor inhibitory functions in healthy elderly that could benefit from aerobic exercise training: specifically, the brain neurotransmission systems and the frontal-basal ganglia network. In conclusion, we raise two fundamental questions which are yet to be addressed: (1) the extent to which different brain neurotransmitter systems are affected by aerobic exercise training; (2) the extent to which neurotransmitter levels prior to the onset of intervention may facilitate (or impede) training-induced neuroplasticity in the aging brain.