Health Economic Evaluations for Alzheimer’s Disease: Pathophysiology, Diagnosis and Pharmacological Approaches

Abstract

Alzheimer's disease (AD) was first described by Alois Alzheimer in 1907 as a slowly progressing form of dementia that affects cognition, behavior, and functional status. It may be identified by the extracellular amyloid b (Ab) plaques as well as neurofibrillary tangle (NFT) deposits that are seen inside the neurons. Early-onset Alzheimer's disease (EOAD) and late-onset Alzheimer's disease (LOAD) are the two main categories that form the base of AD presentation. EOAD is a condition that develops before the age of 65 and is linked to Mendelian inheritance, which results in a mutation in the genes APP, PSEN1, or PSEN2. So it is familial AD. While LOAD occur after age 65 years of age and, it is not  related to a genetic cause. So it is sporadic AD. To assess and monitor the rate and pattern of cognitive loss, screening measures like the MMSE and the Montreal Cognitive Examination are utilized. Clinical biomarker testing is now available to assist physicians in determining the the presence and severity of AD pathologic alterations, as well as their lasting effects. Fibrillar (plaque) amyloid is detectable on PET. Despite the fact that AD is a public health issue, only two pharmaceutical classes—antagonists of N-methyl d-aspartate (NMDA) and inhibitors of the cholinesterase enzyme (naturally occurring, synthetic, and hybrid variants)—are allowed to be practiced to treat AD. AD is brought on by a decrease in the synthesis of acetylcholine (Ach) Increasing acetylcholine levels by decreasing acetylcholinesterase is one of the therapeutic interventions that enhances neuronal cells and cognitive function. Tacrine was the first cholinesterase inhibitor drug authorized by the FDA to be used for the treatment of AD.