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Alzheimer’s disease (AD) is a neuro-degenerative disease, causing gradual decline in memory function in the affected patients. The loss of memory makes their existence miserable. It is first noticed and reported by the patient’s care takers. The clinicians objectively assess the type and degree of the memory loss by a specific battery of tests, specially designed for the purpose (like Montreal Cognitive Assessment (MoCA) test., Mini-Mental State Exam (MMSE etc.)). Understanding the symptoms of AD, arising out of memory loss, requires deeper insights into what initiates the memory (the sensory inputs from the five sense organs), the different types of memories (explicit, implicit memories, their sub types and associative memory etc.), how the memory signals are modified at the level of the neuron, (analog to digital signals) and the synapse (sensitization, habituation and Long term potentiation / depression etc.), the processing that the inputs received , undergo (encoding, consolidation /organization, storage and retrieval) in higher brain centres (amygdala, hippocampus prefrontal vortex etc.) and also the role played by the various receptors (NMDA, AMPA and the kinase receptors), the neurotransmitters (acetylcholine, Norepineprine, Gama aminobutic acid, serotonin etc.), the central network systems involved (central executive network, salience network, and the default mode network). In short, it is the study all about, of the physiology of memory. The next step is to integrate this knowledge to interpret symptoms of patients with AD. Accordingly, the subject under discussion is dealt with in two parts. Firstly, how the memory is affected in AD and secondly the physiology behind these changes.
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