This presentation discussed the intricate relationship between neuroinflammation and neurodegenerative diseases. Sagar Chanderkar began by highlighting that neuroinflammation was a common feature in various neurodegenerative diseases, such as Alzheimer's, Parkinson's, Huntington's disease, and amyotrophic lateral sclerosis (ALS). He explained that protein aggregation contributed to inflammation in the central nervous system and that neuroinflammation could also trigger protein deposition.

Chanderkar noted the significant increase in research and publications on neuroinflammation over the past two decades, indicating a growing interest and evolving understanding in this field. He emphasised that the brain was not an isolated organ but communicated with the peripheral immune system through the blood-brain barrier, interstitial fluid, and the lymphatic system.

The roles of microglia and astrocytes in the brain's immune response were discussed in detail. Microglia acted as protectors by phagocytosing toxins, but chronic activation could lead to brain damage. Astrocytes, part of the glial system, also contributed to the blood-brain barrier and interacted with microglia.

Chanderkar also explored the link between metabolic syndrome, including diabetes and obesity, and neuroinflammation. He explained that early onset of diabetes and obesity could increase the risk of developing dementia and Alzheimer's disease later in life. High levels of peripheral inflammation markers like hs-CRP were also associated with a higher risk of neurodegenerative diseases.

In the latter part of the presentation, Chanderkar focused on Alzheimer's disease, discussing the classical pathophysiologies of amyloid flux, intracellular Tau tangles, and neuronal degeneration. He highlighted the evolving understanding of Alzheimer's, including the role of the complement system and the NLRP3 inflammasome in triggering cytokine and chemokine responses.

Chanderkar concluded by discussing the development of therapies targeting neuroinflammation, including those addressing microglia and astrocytes. He mentioned ongoing trials and the potential for new drugs to target neuroinflammation, emphasising the importance of continued research and development in this field.