Thekkuttuparambil Ananthanarayanan Ajith*
Department of Biochemistry, Amala Institute of Medical Sciences, Amala Nagar, Kerala, India
*Corresponding Author: Thekkuttuparambil Ananthanarayanan Ajith, Professor of Biochemistry, Department of Biochemistry, Amala Institute of Medical Sciences, Amala Nagar, Kerala, India.
Received: September 29, 2020; Published: October 28, 2020
Neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Amyotrophic lateral sclerosis and Huntington’s disease remain a major challenge to human. Among the neurodegenerative diseases, Alzheimer's disease (AD) and Parkinson’s disease are two major forms. According to the recent survey in US, more than 5.5 million (age 65 or older) people have dementia caused by Alzheimer’s and remain the 5th leading cause of death among the elders. World Health Organization (WHO) expected ~ 16.2% prevalence of AD among people over 65 years worldwide by 2050. The median survival of AD patients who diagnosed at age 65 years is estimated to be 9 years. The disease causes ~ 66-75% of household income for the management. Furthermore, due to behavioral disturbances, faecal and urinary incontinence and increase need for personal care of AD patients, prevalence of anxiety and depression were found among caregivers mainly female care givers. Despite large number of studies to find various mechanisms for AD, the exact molecular mechanism in the pathophysiology of this irreversible disease has not yet been established. Formation and deposition of extracellular β-amyloid peptide (Aβ, ~4 kDa protein) in an amyloidogenic pathway in the brain region leading to synaptic dysfunction, disrupting neural connectivity was demonstrated as well . Aβ is formed from the β-amyloid precursor protein after processing by the membrane-bound multi-subunit aspartyl endoprotease, β- (exists in two forms BACE1 and BACE2) and γ-secretase. Presenilin1 or 2 (PS1 or PS2), subunit of γ – secretase was found to be mutated in familiar AD cases. In addition to this, several forms of mutations in the β-amyloid precursor protein were also evidenced. Among the different Aβ species found, the one ending at position 40 (Aβ40) are present in 80 - 90% cases, followed by slightly longer forms Aβ 42 in 5 - 10% cases. Aβ42 are more toxic due to its fibrillogenic and hydrophobic nature.
Citation: Thekkuttuparambil Ananthanarayanan Ajith. “Does Estrogen Therapy Prevent Late Onset Alzheimer's Disease?". Acta Scientific Neurology 3.11 (2020): 105-107.
Copyright: © 2020 Thekkuttuparambil Ananthanarayanan Ajith. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.