Neuroinflammation is a complex immune response in the central nervous system (CNS) which is generally characterized by increased glial (microglia and astrocyte) reactivity, recruitment, and proliferation. Upon activation, glia undergoes structural, morphological, or transcriptional changes which lead to microglial de-ramification and astroglial hypertrophy; hence the threshold of glial reactivity that defines neuroinflammation remains unclear. The glial function can also be both pro-inflammatory and anti-inflammatory, based on the secretion of protective/detrimental mediators and resolution/worsening of tissue damage. On the contrary to the acute inflammation, chronic neuroinflammatory conditions in the CNS can lead to the excessive release of detrimental mediators leading to the dysregulation of myelin integrity, neuronal and axonal injury, resulting in longer-lasting neurological disability. Additionally, these neurological changes increase upon aging. Notably, this inflammatory episode is observed in most neurological diseases including Alzheimer’s disease, Parkinson’s disease, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis, although the pathoetiology of age-related chronic neuroinflammation remains unclear.
While symptomatic treatments using approved therapeutics can improve the quality of life of patients with neurodegenerative diseases, no therapeutics can stop disease progression or provide a cure. Moreover, currently approved medications are associated with the high cost and side effects. Therefore, there is an urgent need to search for new and refined therapeutics, employing chemical and/or non-chemical agents such as alternative and plant-based ethnobotanical medicines. New therapeutic agents must be applied which better understand how to target brain inflammation to lead to the development of new drugs for the treatment of brain diseases involving glial activation and neuroinflammation.
This Research Topic is a collection of studies focused on pharmacological approaches to improve neurodegenerative and neuroinflammatory conditions in both pathology and symptoms studied in both preclinical and clinical settings. This translational effort will be focusing on but not limited to the following topics of interest:
• Impact of pharmacological approaches in the modulation of neuroinflammation; in particular whether therapeutics can modulate microglial and astrocytic functions and morphology.
• Impact of pharmacological approaches in recovery from behavioral/functional deficits.
• Impact of pharmacological approaches in the acceleration of myelin debris phagocytosis and myelination.
• Effect of pharmacological approaches in reducing neuronal and axonal damage.
• Impact of pharmacological approaches in reversing the de-ramification of microglia and astrocyte hypertrophy.
• Effect of pharmacological approaches in reducing disease markers (e.g. amyloid-ß or neurofibrillary tangles in Alzheimer’s disease, a-synuclein in Parkinson’s disease) in neurological diseases.
Neuroinflammation is a complex immune response in the central nervous system (CNS) which is generally characterized by increased glial (microglia and astrocyte) reactivity, recruitment, and proliferation. Upon activation, glia undergoes structural, morphological, or transcriptional changes which lead to microglial de-ramification and astroglial hypertrophy; hence the threshold of glial reactivity that defines neuroinflammation remains unclear. The glial function can also be both pro-inflammatory and anti-inflammatory, based on the secretion of protective/detrimental mediators and resolution/worsening of tissue damage. On the contrary to the acute inflammation, chronic neuroinflammatory conditions in the CNS can lead to the excessive release of detrimental mediators leading to the dysregulation of myelin integrity, neuronal and axonal injury, resulting in longer-lasting neurological disability. Additionally, these neurological changes increase upon aging. Notably, this inflammatory episode is observed in most neurological diseases including Alzheimer’s disease, Parkinson’s disease, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis, although the pathoetiology of age-related chronic neuroinflammation remains unclear.
While symptomatic treatments using approved therapeutics can improve the quality of life of patients with neurodegenerative diseases, no therapeutics can stop disease progression or provide a cure. Moreover, currently approved medications are associated with the high cost and side effects. Therefore, there is an urgent need to search for new and refined therapeutics, employing chemical and/or non-chemical agents such as alternative and plant-based ethnobotanical medicines. New therapeutic agents must be applied which better understand how to target brain inflammation to lead to the development of new drugs for the treatment of brain diseases involving glial activation and neuroinflammation.
This Research Topic is a collection of studies focused on pharmacological approaches to improve neurodegenerative and neuroinflammatory conditions in both pathology and symptoms studied in both preclinical and clinical settings. This translational effort will be focusing on but not limited to the following topics of interest:
• Impact of pharmacological approaches in the modulation of neuroinflammation; in particular whether therapeutics can modulate microglial and astrocytic functions and morphology.
• Impact of pharmacological approaches in recovery from behavioral/functional deficits.
• Impact of pharmacological approaches in the acceleration of myelin debris phagocytosis and myelination.
• Effect of pharmacological approaches in reducing neuronal and axonal damage.
• Impact of pharmacological approaches in reversing the de-ramification of microglia and astrocyte hypertrophy.
• Effect of pharmacological approaches in reducing disease markers (e.g. amyloid-ß or neurofibrillary tangles in Alzheimer’s disease, a-synuclein in Parkinson’s disease) in neurological diseases.