Pharmacological Treatment Strategies for Alzheimer's Disease.
10.5124/jkma.2002.45.4.401
- Author:
Dong Won YANG
- Publication Type:Clinical Trial ; Original Article
- Keywords:
Alzheimer's disease;
Cholinesterase inhibitor;
Beta amyloid peptide;
Dementia
- MeSH:
Aged;
alpha-Tocopherol;
Alzheimer Disease*;
Amyloid;
Autoimmunity;
Celecoxib;
Cholinesterases;
Cognition;
Dementia;
Disease Progression;
Estrogen Replacement Therapy;
Female;
Ginkgo biloba;
Humans;
Immunization;
Methods;
Prednisone;
Rivastigmine;
Tacrine
- From:Journal of the Korean Medical Association
2002;45(4):401-408
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Alzheimer's disease(AD) is one of the most common causes of mental deterioration in elderly individuals, accounting for around 45~60% of the overall cases of dementia over 65 years of age. Although there is presently no "cure" for AD, a large number of potential therapeutic interventions have emerged to correct cholinergic dysfunctions. Currently, cholinergic therapy, particularly cholinesterase inhibition, represents the most realistic approach to the symptomatic treatment of AD. Modest efficacy for mild to moderate AD has been shown in well-designed clinical trials for tacrine, donepezil, rivastigmine, and galantimine. Among other treatment options, estrogen replacement therapy in postmenopausal women is under active investigation, but recent studies showed somewhat disappointing results. Epidemiological and clinical data suggest that nonsteroidal anti-inflammatory drugs are beneficial in the treatment and prevention of AD. But prednisone and COX-2 inhibitor, celecoxib showed no clinical benefit in recent studies. Alpha-tocopherol and gingko biloba showed some beneficial effect in delaying the progression of AD and enhancing cognitive functions. Immunization with beta amyloid peptide was considered to be the only method to prevent and halt disease progression in patients with AD. Recently, phase II clinical trial using synthetic beta amyloid peptide (AN-1792) was discontinued because some patients showed neuro-inflammation which may be caused by autoimmune responses.
