Adam Hoffman
Numerous people are affected by obesity, which is a widespread health issue caused by excessive ingestion of saturated fats, inactivity, or a sedentary lifestyle. Leptin is an adipokine that is released by adipose tissue and rises in obesity. It has central activities in the cerebral cortex, hippocampus, and other areas and nuclei of the Central Nervous System (CNS), in addition to the hypothalamus. These regions are the first to experience chronic neurocognitive deficits including mild cognitive impairment (MCI) and Alzheimer's disease because they express the long form of the leptin receptor LepRb, which is the only leptin receptor capable of conveying complete leptin signals (AD). As leptin resistance is usually linked to obesity, which is a chronic low-grade inflammatory condition, and obesity is thought to be a risk factor for AD, we examine various leptin resistance mechanisms in this review that may be responsible for raising the chance of developing AD. SOCS3, PTP1B, and TCPTP, whose signaling is associated with inflammation and may be exacerbated in AD, are important leptin resistance players. However, certain results are debatable, and further research is required to understand the pathogenic processes that cause AD and how altered leptin signaling influence those processes.