ABSTRACT
Alzheimer’s disease (AD) is a fatal, progressive, and degenerative disease, and is the most common form of dementia worldwide. Cognitive impairment in AD is gradual in onset but constant in progression. The presence of amyloid plaques and neurofibrillary tangles are the two pathological hallmark of Alzheimer’s disease, which are further associated with dysfunctioning of various neurochemical systems, cellular systems, and cell signaling pathways. Neurochemical deficiencies, synaptic dysfunction, and alterations in brain neurotransmitters are thought to be responsible for the cognitive impairment. Therefore, it is of absolute interest to explore neurobiology and neurotransmission in AD. The chapter further explores neurochemical abnormalities in signaling pathways like the Fyn kinase pathway, cyclin-dependent kinase 5 (CDK5), glycogen synthase kinase 3β (GSK-3β), Wnt signaling, the PI3K/Akt/mTOR pathway, the peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α) pathway, and their crosstalk, in order to understand the pathogenesis of AD. Targeting the signaling pathways can revolutionize the treatment of AD and can help in finding a potential treatment strategy for AD in future.
