How do neurons age?A focused review on the aging of the microtubular cytoskeleton

Aging is the leading risk factor for Alzheimer’s disease and other neurodegenerative diseases. We now understand that a breakdown in the neuronal cytoskeleton, mainly underpinned by protein modifications leading to the destabilization of microtubules, is central to the pathogenesis of Alzheimer’s disease. This is accompanied by morphological defects across the somatodendritic compartment, axon, and synapse. However, knowledge of what occurs to the microtubule cytoskeleton and morphology of the neuron during physiological aging is comparatively poor. Several recent studies have suggested that there is an age-related increase in the phosphorylation of the key microtubule stabilizing protein tau, a modification, which is known to destabilize the cytoskeleton in Alzheimer’s disease. This indicates that the cytoskeleton and potentially other neuronal structures reliant on the cytoskeleton become functionally compromised during normal physiological aging. The current literature shows age-related reductions in synaptic spine density and shifts in synaptic spine conformation which might explain age-related synaptic functional deficits. However, knowledge of what occurs to the microtubular and actin cytoskeleton, with increasing age is extremely limited. When considering the somatodendritic compartment, a regression in dendrites and loss of dendritic length and volume is reported whilst a reduction in soma volume/size is often seen. However, research into cytoskeletal change is limited to a handful of studies demonstrating reductions in and mislocalizations of microtubule-associated proteins with just one study directly exploring the integrity of the microtubules. In the axon, an increase in axonal diameter and age-related appearance of swellings is reported but like the dendrites, just one study investigates the microtubules directly with others reporting loss or mislocalization of microtubule-associated proteins. Though these are the general trends reported, there are clear disparities between model organisms and brain regions that are worthy of further investigation. Additionally, longitudinal studies of neuronal/cytoskeletal aging should also investigate whether these age-related changes contribute not just to vulnerability to disease but also to the decline in nervous system function and behavioral output that all organisms experience. This will highlight the utility, if any, of cytoskeletal fortification for the promotion of healthy neuronal aging and potential protection against age-related neurodegenerative disease. This review seeks to summarize what is currently known about the physiological aging of the neuron and microtubular cytoskeleton in the hope of uncovering mechanisms underpinning age-related risk to disease.

The Distribution and Morphological Diversity of GABA-containing Neurons in The Prefrontal Cortex of Human Newborn Baby Infant

The prefrontal cortex of a human full termnewborn infant just after accidental death was studies by mcans of immunocytochemical technique with antibody directedagainst GABA(Immunonuclear Corp.)and ABC kit(Vector)。GABA-containing neurons were found over all layers and all were nonpyramidal cells.The laminar distribution of GABA-containing ne-urons was not even between different layers,density in laye Ⅱ was prominently higher than any other layers,density in layer Ⅲ and layer Ⅳ was higher than that in layer V and Ⅵ.

Three-dimensional histology:new visual approaches to morphological changes during neural regeneration

Three-dimensional（3D） histology utilizes tissue clearing techniques to turn intact tissues transparent,allowing rapid interrogation of tissue architecture in three dimensions.In this article,we summarized the available tissue clearing methods and classified them according to their physicochemical principles of operation,which provided a framework for one to choose the best techniques for various research settings.Recent attempts in addressing various questions regarding the degenerating and regenerating nervous system have been promising with the use of 3D histological techniques.

Anti-aging effects of moxa cone moxibustion As a free radical scavenger complement

Therapies that complement free radical scavenging are an important approach for treating aging in the brain. In the present study, two formulations of moxa cone moxibustion were applied at acupoints Zusanfi （ST 36） and Xuanzhong （GB 39）, and at acupoints Baihui （DU 20） and Guanyuan （RN 4）, in D-galactose-induced senile mice. The results revealed that moxa cone moxibustion improved total superoxide dismutase and Cu/Zn-superoxide dismutase activity in the homogenates of the cerebral tissue, as well as ameliorating deficits in neuronal morphology and neuronal density in the cerebral cortex and hippocampal CA3. Moxa cone moxibustion also enhanced learning and memory functions of senile mice. Moxa cone moxibustion at Zusanli, Xuanzhong, Baihuiand Guanyuan acupoints can thus be used to complement free radical scavengers, with efficacy that is equal to that of electroacupuncture at Zusanliand Xuanzhong, and superior to that of nimodipine treatment.