Induced Impairment of Neurogenesis and Brain Diseases
The impairment of neurogenesis may be induced after pre- and post-natal chemical and biological toxin, alcohol, or radiation exposure, drug treatment, hormone imbalances, stress, pain, hypoxia, brain trauma, malnutrition, and aging. It also occurs as a result of genetic disorders such as Down syndro...
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Format: | Electronic Book Chapter |
Language: | English |
Published: |
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MDPI - Multidisciplinary Digital Publishing Institute
2023
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Online Access: | DOAB: download the publication DOAB: description of the publication |
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Summary: | The impairment of neurogenesis may be induced after pre- and post-natal chemical and biological toxin, alcohol, or radiation exposure, drug treatment, hormone imbalances, stress, pain, hypoxia, brain trauma, malnutrition, and aging. It also occurs as a result of genetic disorders such as Down syndrome (DS), autism, fragile X syndrome (FXS), neurological disorders including Alzheimer's disease (AD), Parkinson's disease (PD) epilepsy, and Huntington's disease (HD), and neuropsychiatric disorders such as depression and schizophrenia; however, the causal relationship between the impairment of neurogenesis and neurological and neuropsychiatric disorders remains unknown. In this Special Issue, entitled "Induced Impairment of Neurogenesis and Brain Diseases", original animal or cell experimental research and review papers were combined to discuss different causes of the impairment of neurogenesis, relevant neurobehavioral changes, molecular mechanisms, and therapeutic approaches. The aim is to update researchers and clinicians about the complexity of the development of the impairment of neurogenesis, the importance of the involvement of the impairment of neurogenesis in neurological and neuropsychiatric disorders, and to provide some clues for designing novel therapeutic approaches by targeting the impairment of neurogenesis to effectively prevent or treat different genetic, neurological, and neuropsychological disorders. |
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Physical Description: | 1 electronic resource (282 p.) |
ISBN: | books978-3-0365-6213-1 9783036562148 9783036562131 |
Access: | Open Access |