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Albeit any aberration in the mechanisms associated with transmission of these signals leads to loss of synaptic contacts in both the neocortex and hippocampus thereby causing insidious cognitive decline and memory dysfunction. Compelling evidence suggests that soluble amyloid-\u03b2 (A\u03b2) and hyperphosphorylated tau serve as toxins in the dysfunction of synaptic plasticity and aberrant neurotransmitter (NT) release at synapses consequently causing a\u00a0cognitive decline in Alzheimer\u2019s disease (AD). Further, an imbalance between excitatory and inhibitory neurotransmission systems induced by impaired redox signaling and altered mitochondrial integrity is also amenable for such abnormalities. Defective NT release at the synaptic junction causes several detrimental effects associated with altered activity of synaptic proteins, transcription factors, Ca\n                    <jats:sup>2+<\/jats:sup>\n                    homeostasis, and other molecules critical for neuronal plasticity. These detrimental effects further disrupt the normal homeostasis of neuronal cells and thereby causing synaptic loss. Moreover, the precise mechanistic role played by impaired NTs and neuromodulators (NMs) and altered redox signaling in synaptic dysfunction remains mysterious, and their possible interlink still needs to be investigated. Therefore, this review elucidates the intricate role played by both defective NTs\/NMs and altered redox signaling in synaptopathy. Further, the involvement of numerous pharmacological approaches to compensate neurotransmission imbalance has also been discussed, which may be considered as a\u00a0potential therapeutic approach in synaptopathy associated with AD.\n                  <\/jats:p>","DOI":"10.3233\/jad-160623","type":"journal-article","created":{"date-parts":[[2016,9,23]],"date-time":"2016-09-23T10:31:57Z","timestamp":1474626717000},"page":"1017-1039","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":41,"title":["Stress-Induced Synaptic Dysfunction and\u00a0Neurotransmitter Release in\u00a0Alzheimer\u2019s Disease: Can Neurotransmitters and Neuromodulators be\u00a0Potential Therapeutic Targets?"],"prefix":"10.1177","volume":"57","author":[{"given":"Saurabh Kumar","family":"Jha","sequence":"first","affiliation":[{"name":"Department of Biotechnology, Molecular Neuroscience and Functional Genomics Laboratory, Delhi Technological University 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