@entity15 and @entity195 are fundamentally different diseases. However, recent data suggest that certain mechanisms of @entity179 may be shared between the two diseases. Inflammation drives the disease in @entity15 . It is also present in @entity195 lesions, where it may have dual functions in amyloid clearance as well as in the propagation of @entity179 . In both diseases, @entity528 , axons, and synapses occur on the background of profound @entity2383 . Reactive @entity26 and @entity842 intermediates are major candidates for the induction of @entity2383 . Radicals are produced through the induction of the respiratory burst in activated microglia, which are present in the lesions of both diseases. In addition, liberation of toxic @entity68 from intracellular stores may augment radical formation. Finally reactive @entity26 species are also produced in the course of @entity2383 itself. Anti-oxidant and mitochondria protective therapeutic strategies may be beneficial both in @entity15 and @entity195 in particular in early stages of the disease.

Mechanisms of @entity179 shared between XXXX and @entity195 .

@entity26 :: ('MESH:D010100', 'Chemical') :: ['oxygen'] @entity179 :: ('MESH:D019636', 'Disease') :: ['neurodegeneration'] @entity842 :: ('MESH:D009569', 'Chemical') :: ['nitric oxide'] @entity195 :: ('MESH:D000544', 'Disease') :: ["Alzheimer's disease"] @entity15 :: ('MESH:D009103', 'Disease') :: ['Multiple sclerosis', 'multiple sclerosis'] @entity528 :: ('MESH:D009410', 'Disease') :: ['degeneration of neurons'] @entity68 :: ('MESH:D007501', 'Chemical') :: ['iron'] @entity2383 :: ('MESH:D028361', 'Disease') :: ['mitochondrial injury']
@entity15 :: (MESH:D009103,Disease) :: ['multiple sclerosis']
