Due to the increase in life expectancy, the incidence of age-associated diseases has dramatically increased in recent decades. Thus, the interest in understanding the molecular mechanisms regulating these disorders has exponentially increased in the last years. Among them, neurodegenerative diseases are one of the most disabling pathologies, with high healthcare costs for National Health Systems and patient families. Current research suggests that neuroinflammation plays a prominent role in neurodegenerative pathologies of diverse etiology, placing this phenomenon as a potential therapeutic target, common to different diseases. Among the different immune cells that characterize neuroinflammation, microglial cells are by far the most studied and characterized cells. However, recent advances suggest that the infiltration of T cells and neutrophils could decisively contribute to pathologies like Alzheimer’s disease, Amyotrophic Lateral Sclerosis or Parkinson’s disease.
The appearance of changes in both the abundance and the activation status of different immune cell populations during neurodegeneration is well characterized. Nevertheless, still little is known about the molecular changes driving these features. Altered phagocytosis of neurotoxic proteins, increased activation of pro-inflammatory pathways driven by molecules such as NF-KB, p38 or JNK are common features observed in microglial cells during neurodegeneration. Additionally, epigenetic regulation of immune cell status is emerging as a new field with important implications in neurodegenerative diseases. Therefore, this Research Topic will focus on molecular and epigenetic mechanisms driving neuroinflammation in age-related diseases.
We especially welcome article submissions on, but not limited to, the following topics:
• Altered epigenetic hallmarks, both at DNA and protein levels, occurring in immune cells during neurodegenerative diseases
• Altered metabolic or signaling pathways driving immune cell activation during neurodegeneration
• Studies characterizing specific populations of immune cells with new roles in driving neurodegeneration
• New loss or gain of function mechanisms in immune cells that contribute to neuronal death
Due to the increase in life expectancy, the incidence of age-associated diseases has dramatically increased in recent decades. Thus, the interest in understanding the molecular mechanisms regulating these disorders has exponentially increased in the last years. Among them, neurodegenerative diseases are one of the most disabling pathologies, with high healthcare costs for National Health Systems and patient families. Current research suggests that neuroinflammation plays a prominent role in neurodegenerative pathologies of diverse etiology, placing this phenomenon as a potential therapeutic target, common to different diseases. Among the different immune cells that characterize neuroinflammation, microglial cells are by far the most studied and characterized cells. However, recent advances suggest that the infiltration of T cells and neutrophils could decisively contribute to pathologies like Alzheimer’s disease, Amyotrophic Lateral Sclerosis or Parkinson’s disease.
The appearance of changes in both the abundance and the activation status of different immune cell populations during neurodegeneration is well characterized. Nevertheless, still little is known about the molecular changes driving these features. Altered phagocytosis of neurotoxic proteins, increased activation of pro-inflammatory pathways driven by molecules such as NF-KB, p38 or JNK are common features observed in microglial cells during neurodegeneration. Additionally, epigenetic regulation of immune cell status is emerging as a new field with important implications in neurodegenerative diseases. Therefore, this Research Topic will focus on molecular and epigenetic mechanisms driving neuroinflammation in age-related diseases.
We especially welcome article submissions on, but not limited to, the following topics:
• Altered epigenetic hallmarks, both at DNA and protein levels, occurring in immune cells during neurodegenerative diseases
• Altered metabolic or signaling pathways driving immune cell activation during neurodegeneration
• Studies characterizing specific populations of immune cells with new roles in driving neurodegeneration
• New loss or gain of function mechanisms in immune cells that contribute to neuronal death
