TY - JOUR
T1 - Therapeutic approaches to the treatment of Alzheimer's disease
AU - Yamada, Kiyofumi
AU - Toshitaka, Nabeshima
PY - 2002/9/1
Y1 - 2002/9/1
N2 - Alzheimer's disease is the most common cause of progressive decline of cognitive function in aged humans and is characterized by the presence of numerous senile plaques and neurofibrillary tangles accompanied by neuronal loss. The only treatment currently available for the disease is pharmacotherapy with acetylcholinesterase inhibitors, a palliative strategy aimed at the temporary improvement of cognitive function. Other strategies with disease-modifying potential may include the use of antiinflammatory drugs, estrogen replacement therapy and antioxidants. Recent progress in understanding the molecular and cellular pathophysiology of Alzheimer's disease has suggested possible pharmacological interventions that could modify the development and progress of the disease (disease-modifying therapy), such as treatment with secretase inhibitors, transition metal chelators, HMG-CoA reductase inhibitors and amyloid-β immunization. Inhibitors of tau hyperphosphorylation may also modulate the development and progress of the disease.
AB - Alzheimer's disease is the most common cause of progressive decline of cognitive function in aged humans and is characterized by the presence of numerous senile plaques and neurofibrillary tangles accompanied by neuronal loss. The only treatment currently available for the disease is pharmacotherapy with acetylcholinesterase inhibitors, a palliative strategy aimed at the temporary improvement of cognitive function. Other strategies with disease-modifying potential may include the use of antiinflammatory drugs, estrogen replacement therapy and antioxidants. Recent progress in understanding the molecular and cellular pathophysiology of Alzheimer's disease has suggested possible pharmacological interventions that could modify the development and progress of the disease (disease-modifying therapy), such as treatment with secretase inhibitors, transition metal chelators, HMG-CoA reductase inhibitors and amyloid-β immunization. Inhibitors of tau hyperphosphorylation may also modulate the development and progress of the disease.
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U2 - 10.1358/dot.2002.38.9.696538
DO - 10.1358/dot.2002.38.9.696538
M3 - Review article
C2 - 12582450
AN - SCOPUS:0036750190
VL - 38
SP - 631
EP - 637
JO - Drugs of Today
JF - Drugs of Today
SN - 0025-7656
IS - 9
ER -