Mutational, Docking and Simulation Studies on SERPINI1 Gene and Its Experimental Assay With Ascorbic Acid for Its Role in Alzheimers Disease

Abstract

A healthy human brain consists of 86 billion neurons. The points of junction where these neurons communicate are termed as synapses[1]. Synapses transmit information from post-synaptic neuron to pre-synaptic neuron in the form of neurotransmitters. Effectual communication can be achieved by neurons through strengthening the molecular structure of synapses [2]. In normal brain, aging leads to weakening of synapses by down regulating the speed of connection within neurons and compromises with memory, decision making skills of an individual. However, in Alzheimer’s functioning of neurons can be lost. Alzheimer’s Disease (AD) AD is a neurodegenerative disorder which impairs memory of an individual and is a protein conformational disease (PCD) caused due to abnormal folding of soluble proteins present in the brain [3], [4]. AD is marked by the presence of amyloid-beta plaques and neurofibrillary tangles in the medial temporal lobe of the brain [5] History AD was first reported by Alois Alzheimer while working on a patient named Auguste Deter in Mental Hospital of Frankfurt. Following her death, brain biopsy was conducted in order to identify the relation between the records maintained in successive 4 years and her symptoms. He discovered that the part of the brain which controls thinking, memory, judgment, language was severely damaged. Formation of senile plaques and tangles were observed in neurons and nerve fibers. While presenting in the conference of southwestern Germany, he reported the results of the brain biopsy and symptoms. A local neurological symptom, delusion hallucinations were among the patient symptoms [6]. In this way AD was discovered.