ALZHEIMER’S DISEASE: PATHOLOGICAL HALLMARKS OF ALZHEIMER’S DISEASE

Dementia is a collection of symptoms, including memory loss and cognitive impairment, that cause neuronal disruption and lead to certain mental illnesses. The most common cause of dementia is Alzheimer’s disease (AD). Potential causes of illness extension include tau aggregation, amyloid beta build-up outside of neurons, and the formation of neurofibrillary tangles (NFTs) inside neurons. At one point in time, Alzheimer’s disease was the most common illness worldwide. The majority of research indicates that ROS (Reactive Oxygen Species) play a significant role in neurodegeneration and, eventually, Alzheimer’s disease. Amyloid-peptide increases in Alzheimer’s disease led to an increase in ROS production, which kills neurons. A transcription factor called Farnesoid X Receptor (FXR) regulates inflammation, oxidative stress (OS), and the brain’s metabolism of fats and carbohydrates. Nuclear erythroid 2 related factor 2 (Nrf2) is a transcription factor that regulates the production of many antioxidant genes and is an essential regulator of neural defence against OS. According to certain studies, Nrf2 activation can regulate the expression and activity of FXR in the liver, suggesting that these two transcription factors work in concert. Even while the exact relationship between FXR and Nrf2 in the brain is not entirely understood, it is likely that comparable interactions occur in this case. Activating the FXR and Nrf2 pathways may, in general, decrease oxidative stress and inflammation in the brain, making them appealing therapeutic targets for neurological disorders associated with inflammation and OS.