I Alzheimer’s disease
　　Alzheimer’s type is the commonest form of dementia, the other forms being vascular dementia (VaD) and mixed dementia. Alzheimer’s disease (AD) has been classified and managed as a neurodegenerative disease characterized by extracellular amyloid plaques and intracellular neurofibrillary tangles (Table 1). On the other hand, VaD is caused by vascular lesions, cerebral infarctions, multiple lacunar infarctions and ischemic periventricular leukoencephalopathy (Table 1).
　　AD is defined pathologically by extracellular neuritic plaques comprised of fibrillar deposits of a 4 kDa hydrophobic polypeptide known as β-amyloid (Aβ) and neurofibrillary tangles consisting of paired helical filaments of hyperphosphorylated tau (Figure 1). Fibrillar Aβ (fAβ) generates reactive oxygen species (ROS) , which cause membrane lipid peroxidation and disturb the integrity of neuronal membranes. These free radicals stimulate L-typte voltage-sensitive Ca²⁺ channel (L-VSCC), and potentiate the influx of Ca²⁺ into neurons. The increment in intracellura Ca²⁺ concentration ([Ca²⁺]i) affects Ca²⁺ -dependent enzymes including cytosolic phospholipase A₂ (cPLA₂), nuclease, kinase and protease. These enzymes are involved in fAβ-induced neuronal cell death, which is typified by several features characteristic of apoptosis. Besides Ca²⁺-dependent protein kinases, fAβ stimulates various kinases including mitogen-activated protein kinase (MAPK) and glycogen synthase kinase (GSK). MAPK phosphorylates and activates cPLA₂, and mediates apoptosis. GSK phosphorylates tau protein, and the hyperphosphorylated tau protein form neurofibrillary tangles resulting in the impaird axonal transport. The neurofibrillary tangles (paired helical filaments of microtubules and hyper-phosphorylated tau proteins) are the major pathological lesions in an AD brain.