Free radicals in Alzheimer's disease

Alzheimer's disease is a neurodegenerative disorder comprising multisystem atrophies probably caused by multifactorial processes. The disease is chara cterized by typical neuropathology, impaired synaptic function and massive cell loss. The pathobiochemistry of this disorder involves oxidative stress , which accumulates free radicals leading to excessive lipid peroxidation a nd neuronal degeneration in certain brain regions. Moreover, radical induce d disturbances of DNA, proteins and lipid membranes have been measured. The hypothesis has been proposed that cellular events involving oxidative stre ss may be one basic pathway leading to neurodegeneration in Alzheimer's dis ease. In this work we report evidence for increased oxidative stress and di sturbed defense mechanisms in Alzheimer's disease, which may result in a se lf-propagating cascade of neurodegenerative events. Furthermore it is evide nt from experimental data, that aggregation of beta-amyloid and beta-amyloi d toxicity is favourably caused by oxidative stress. Therefore, oxidative s tress plays a key role in the conversion of soluble to unsoluble beta-amylo id, suggesting that oxidative stress is primary to the beta-amyloid cascade .