Past and Future of Drug Treatments for Alzheimer's Disease
10.4306/jknpa.2018.57.1.30
- Author:
Seong Yoon KIM
1
Author Information
1. Department of Psychiatry, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. sykim@amc.seoul.kr
- Publication Type:Review
- Keywords:
Alzheimer's disease;
Drug;
Amyloid;
Tau;
Acetyl-choline esterase inhibitors
- MeSH:
Alzheimer Disease;
Amyloid;
Anti-Inflammatory Agents;
Biomarkers;
Brain;
Dementia;
Estrogens;
Ginkgo biloba;
Hope;
Humans;
Hydroxymethylglutaryl-CoA Reductase Inhibitors;
Immunization, Passive;
Pathology;
Vitamins
- From:Journal of Korean Neuropsychiatric Association
2018;57(1):30-42
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
This study reviews evidence for the use of acetyl-choline esterase inhibitors (AChEIs) in treating Alzheimer's patients for the past decades. Even though large number of clinical trials have been conducted to prove the efficacy of these drugs in various clinical situations, questions remain to be answered due to the use of heterogeneous subject population, trial designs, and measurement tools in these studies. Many drugs with unproven clinical benefits, including vitamins, ginko biloba extracts, anti-inflammatory agents, estrogen hormone, and statins, are commonly prescribed in real-world settings for dementia patients. Despite the lack of clinical benefits statistically proven by clinical trials or meta-analyses, anecdotal dramatic improvements in some patients may foster such practices. A further look into why some patients benefit from these medications, while other don't, may shed light on future individually tailored medicine for dementia patients. This study provides a brief review of currently existing immuno-therapeutics in the hope that we can learn from the failures of the amyloid-based active and passive immunization. Issues that we need to address for the successful development of new anti-AD drugs include : 1) the brain pathology precedes clinical symptoms by several decades, 2) we need biological markers that reliably reflect cognitive or functional impairment of AD patients, and 3) we need more detailed and plausible explanations for our brain immune responses and neurodegenerative changes.
