Role of Mitochondria in Alzheimer ́s Disease

Abstract

Alzheimer's disease is the most common neurodegenerative disorder worldwide characterized by considerable atrophy and an enlargement and coarsening of the sulci, amyloid formation in neuritic plaques and brain vessels (amyloid angiopathy), neurofibrillary tangles, and neuronal loss, particularly in the limbic and association cortices. In addition, deficits in cholinergic transmission and associated loss of cholinergic cell bodies, granulovacuolar degeneration and rod-shaped eosinophilic inclusions (Hirano bodies) are common in Alzheimer’s disease patients. Clinical symptoms are characterized by progressive worsening of memory, and cognitive impairment accompanied by one of the following symptoms: aphasia, apraxia, agnosia and disorders in the executive function (Selkoe, 2004). The pathophysiological mechanisms that underlie the neurodegenerative characteristic of Alzheimer's disease are yet to be completely understood, although many factors in disease pathogenesis have been identified, and several theories are emerged. In the last years, mitochondrial dysfunction has been considered as a potential factor implicated at some stage of the pathogenic process (Anandatheerthavarada et al., 2003; Sullivan & Brown, 2005;