Update on Disease-Modifying/Preventive Therapies in Alzheimer’s Disease

Abstract

Alzheimer’s disease (AD) is increasingly becoming a major health problem throughout the US and Western Europe. As the remnants of the Baby Boom generation begin to reach their seniority at the turn of the twenty-first century, the disease has been unwillingly brought to the attention of the public eye. A disease that has traditionally been associated with an aging population has thus become a heated topic of discussion as modern research attempts to prevent and treat this major health burden and plague of the next decade.

Novel strategies for Alzheimer's disease treatment: An overview of anti-amyloid beta monoclonal antibodies

“…[1] AD can exist in two variants, including the more common late-onset AD and an early-onset AD. [1] Present treatments available for AD are limited to symptomatic management that consist mostly of acetylcholinesterase inhibitors (including donepezil, galantamine, and rivastigmine) and the N-methyl-D-aspartate receptor antagonist - memantine). Prognosis in AD is poor, and thus, novel therapies for AD are certainly needed in a growing population of elderly patients or among asymptomatic individuals, who are at risk for AD, worldwide.…”

“…Prognosis in AD is poor, and thus, novel therapies for AD are certainly needed in a growing population of elderly patients or among asymptomatic individuals, who are at risk for AD, worldwide. [1] Current research studies are focused on exploring potential innovative therapies, to assess whether or not it is possible to modify the AD course. If the future treatments, designed to reduce the risk, postpone or even prevent the clinical onset of AD are going to be found, then the most accurate methodology to diagnose AD in the early stage, and to assess the safety and effectiveness of emerging AD treatments (including psychometric tests, biomarkers, procedures to expedite the initiation, and conduction of AD trials), as well as a large number of well-matched participants for these studies will be necessary.…”

“…[2] Moreover, a recent knowledge about the AD pathology, and its specific genes and biomarkers can help stratify many asymptomatic individuals (often unaware of their AD risk) into groups with higher or lower risk of further cognitive deterioration, or full-blown dementia of AD or other types. [12]…”

“…This is related to the fact that the roots of AD are likely to go back decades before the afflicted individuals present with the first symptoms of the disease, and the traditional cognitive outcomes developed for clinical trials in AD are not well suited for the prevention AD trials. [12] Pathological processes in the brain of patients with AD start silently (approximately 10–20 years before any clinical manifestation), and so establishing an early diagnosis of AD, possibly in its prodromal stage, or among asymptomatic individuals, harboring AD-related genetic mutations, is extremely important. It is crucial to identify patients who have some risk factors for AD (e.g.…”

“…[4] Amyloid-beta and tau protein, as a “signature” of AD, have inspired modern research to develop some immunotherapeutic strategies, in attempt to slow down or postpone the disease process. [15] Senile plaques consist of a proteinaceous core, composed of amyloid fibrils, surrounded by dystrophic neurons, astrocytes, and microglial cells. The amyloid precursor protein (APP) is cleared enzymatically by beta secretase and gamma secretase.…”