About this Research Topic
Global statistics show that the median human age had increased from 21.5 years in 1970 to over 30 years in 2019. The global population breakdown by age shows that 26% are younger than 14 years, 8% are older than 65 and the aging population is predicted to expand by over 100%. At the neurological level, aging is associated with a gradual decline of cognitive and motor functions as well as metabolic, cellular, and vascular abnormalities. Structurally, the human brain decreases in weight and volume, in particular after the age of 50. Such morphological changes are generally associated with a loss of neurons and myelinated axons together with increased glial cell number and a high immunoreactivity for astrocytic and microglial markers.
Through this Research Topic, we aim to shed light on the recent advances related to the involvement of glia; particularly microglia, astroglia, and oligodendrocytes, during the aging process and neurodegenerative diseases. We will also emphasize the morpho-functional changes which occur in these glial cells during aging and the development of the diseases. The susceptibility of different brain regions to diseases is a possible result of the overstimulation of signals related to the immune system during aging. Additionally, we will focus on the negative damaging impact of these cascades on different microglial populations depending on the brain area. Moreover, special interest will be given to the therapeutic approaches by targeting glial cells modulation through senescence and up-regulation prevention.
In this Research Topic we welcome authors focusing on:
1- Role of microglia in brain aging and neurodegenerative disorders including Parkinson’s disease, Alzheimer’s disease, Multiple sclerosis, Amyotrophic Lateral Sclerosis, and Huntington’s disease
2- Involvement of astroglia in brain aging and neurodegenerative diseases
3- Morpho-functional impairments of oligodendrocytes during the aging process
4- In vivo and in vitro studies on oligodendrocytes deregulation during aging and neurodegenerative diseases
5- Microglia senescence in the aging brain and the underlying mechanisms
6- Targeting features of microglia senescence as a feasible therapeutic strategy
Through this Research Topic, we aim to shed light on the recent advances related to the involvement of glia; particularly microglia, astroglia, and oligodendrocytes, during the aging process and neurodegenerative diseases. We will also emphasize the morpho-functional changes which occur in these glial cells during aging and the development of the diseases. The susceptibility of different brain regions to diseases is a possible result of the overstimulation of signals related to the immune system during aging. Additionally, we will focus on the negative damaging impact of these cascades on different microglial populations depending on the brain area. Moreover, special interest will be given to the therapeutic approaches by targeting glial cells modulation through senescence and up-regulation prevention.
In this Research Topic we welcome authors focusing on:
1- Role of microglia in brain aging and neurodegenerative disorders including Parkinson’s disease, Alzheimer’s disease, Multiple sclerosis, Amyotrophic Lateral Sclerosis, and Huntington’s disease
2- Involvement of astroglia in brain aging and neurodegenerative diseases
3- Morpho-functional impairments of oligodendrocytes during the aging process
4- In vivo and in vitro studies on oligodendrocytes deregulation during aging and neurodegenerative diseases
5- Microglia senescence in the aging brain and the underlying mechanisms
6- Targeting features of microglia senescence as a feasible therapeutic strategy
Keywords: Neuroinflammation, gliopathy, aging, brain diseases
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
