Microglia and Brain Disorders: The Role of Vitamin D and Its Receptor.
Alessandra MirarchiElisabetta AlbiTommaso BeccariCataldo ArcuriPublished in: International journal of molecular sciences (2023)
Accounting for 5-20% of the total glial cells present in the adult brain, microglia are involved in several functions: maintenance of the neural environment, response to injury and repair, immunesurveillance, cytokine secretion, regulation of phagocytosis, synaptic pruning, and sculpting postnatal neural circuits. Microglia contribute to some neurodevelopmental disorders, such as Nasu-Hakola disease (NHD), Tourette syndrome (TS), autism spectrum disorder (ASD), and schizophrenia. Moreover, microglial involvement in neurodegenerative diseases, such as Alzheimer's (AD) and Parkinson's (PD) diseases, has also been well established. During the last two decades, epidemiological and research studies have demonstrated the involvement of vitamin D3 (VD3) in the brain's pathophysiology. VD3 is a fat-soluble metabolite that is required for the proper regulation of many of the body's systems, as well as for normal human growth and development, and shows neurotrophic and neuroprotective actions and influences on neurotransmission and synaptic plasticity, playing a role in various neurological diseases. In order to better understand the exact mechanisms behind the diverse actions of VD3 in the brain, a large number of studies have been performed on isolated cells or tissues of the central nervous system (CNS). Here, we discuss the involvement of VD3 and microglia on neurodegeneration- and aging-related diseases.
Keyphrases
- neuropathic pain
- autism spectrum disorder
- inflammatory response
- resting state
- cerebral ischemia
- white matter
- induced apoptosis
- functional connectivity
- cell cycle arrest
- endothelial cells
- attention deficit hyperactivity disorder
- bipolar disorder
- spinal cord
- spinal cord injury
- gene expression
- blood brain barrier
- preterm infants
- intellectual disability
- brain injury
- subarachnoid hemorrhage
- lipopolysaccharide induced
- signaling pathway
- cerebrospinal fluid
- endoplasmic reticulum stress