Abstract 2135 Role of Long Non-Coding RNAs in Neuroinflammation and Neurodegenerative diseases

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by dementia, memory loss, and cognitive and behavioral impairment, caused by accumulation of amyloid-beta (Aꞵ) plaques and neurofibrillary tangles. According to the WHO, an estimated 7 million Americans, and 50 million people worldwide are affected by AD. Inflammation mediated by microglia, the resident immune cell in the brain, is thought to play a central role in the development and progression of AD. A growing body of evidence suggests that brain derived neurotrophic factor (BDNF) is one of the key players in maintaining synaptic plasticity in learning and cognition. BDNF plays a crucial role in growth, development, and maintenance of neurons (nerve cells) in the brain. It is found in decreased levels in neuronal diseases like Alzheimer's disease. Recently we have discovered that BDNF expression is regulated by long non-coding RNA (LncRNA) HOTAIR. In the current study we aim to investigate novel LncRNAs associated with Aꞵ induced neuroinflammation, microglial activation and Alzheimer's disease. Our studies have shown that Aꞵ induced neuroinflammation downregulates BDNF in microglia. In a separate study on human THP1-derived macrophages (THP1-Mᶲ) we have identified a panel of novel LncRNAs involved in inflammation, some of which are predicted to be associated with neuroinflammation. In the current research we aim to investigate the mechanism of Aꞵ induced neuroinflammation regulated by these novel lncRNAs. In conclusion, our research may offer new insights into the signaling pathways of neuroinflammation and contribute to the development of potential novel diagnostic and therapeutic strategies.