Memory related molecular signatures: The pivots for memory consolidation and Alzheimer's related memory decline |
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Institution: | 1. Protein Assembly Laboratory, Department of Medical Entomology and Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi 110062, India;2. Department of Molecular Medicine, School of Interdisciplinary Studies, Jamia Hamdard, New Delhi 110062, India;1. Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi 110062, India;2. Division of Basic Medical Sciences, Indian Council of Medical Research, Government of India, V. Ramalingaswamy Bhawan, New Delhi 110029, India;3. Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Jamia Hamdard, New Delhi 110062, India |
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Abstract: | Age-related cognitive decline is the major cause of concern due to its 70% more incidence than dementia cases worldwide. Moreover, aging is also the major risk factor of Alzheimer's disease (AD), associated with progressive memory loss. Approx. 13 million people will have Alzheimer-related memory decline by 2050. Learning and memory is the fundamental process of brain functions. However, the mechanism for the same is still under investigation. Thus, it is critical to understand the process of memory consolidation in the brain and extrapolate its understanding to the memory decline mechanism. Research on learning and memory has identified several molecular signatures such as Protein kinase M zeta (PKMζ), Calcium/calmodulin-dependent protein kinase II (CaMKII), Brain-derived neurotrophic factor (BDNF), cAMP-response element binding protein (CREB) and Activity-regulated cytoskeleton-associated protein (Arc) crucial for the maintenance and stabilization of long-term memory in the brain. Interestingly, memory decline in AD has also been linked to the abnormality in expressing these memory-related molecular signatures. Hence, in the present consolidated review, we explored the role of these memory-related molecular signatures in long-term memory consolidation. Additionally, the effect of amyloid-beta toxicity on these molecular signatures is discussed in detail. |
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Keywords: | Aging Long-term memory Plasticity related proteins Amyloid beta Cognitive deficits |
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