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J Neural Transm. 2011 May;118(5):747-52. Epub 2011 Mar 5.

Mechanisms of neurodegeneration shared between multiple sclerosis and Alzheimer's disease.

Lassmann H.

Center for Brain Research, Medical University of Vienna, Wien, Austria.

Abstract

Multiple sclerosis and Alzheimer's disease are fundamentally different diseases. However, recent data suggest that certain mechanisms of neurodegeneration may be shared between the two diseases. Inflammation drives the disease in multiple sclerosis. It is also present in Alzheimer's disease lesions, where it may have dual functions in amyloid clearance as well as in the propagation of neurodegeneration. In both diseases, degeneration of neurons, axons, and synapses occur on the background of profound mitochondrial injury. Reactive oxygen and nitric oxide intermediates are major candidates for the induction of mitochondrial injury. 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 iron from intracellular stores may augment radical formation. Finally reactive oxygen species are also produced in the course of mitochondrial injury itself. Anti-oxidant and mitochondria protective therapeutic strategies may be beneficial both in multiple sclerosis and Alzheimer's disease in particular in early stages of the disease.

Inflammation drives MS? This paper is worthless.

A prominent clinical symptom in multiple sclerosis (MS), a progressive disorder of the central nervous system (CNS) due to heightened neuro-inflammation, is learning and memory dysfunction.
Here, we investigated the effects of a ketogenic diet (KD) on memory impairment and CNS-inflammation in a murine model of experimental autoimmune encephalomyelitis (EAE), using electrophysiological, behavioral, biochemical and in vivo imaging approaches.
Behavioral spatial learning deficits were associated with motor disability in EAE mice, and were observed concurrently with brain inflammation.
The KD improved motor disability in the EAE model, as well as CA1 hippocampal synaptic plasticity (long-term potentiation) and spatial learning and memory (assessed with the Morris Water Maze).
Moreover, hippocampal atrophy and periventricular lesions in EAE mice were reversed in KD-treated EAE mice.
Finally, we found that the increased expression of inflammatory cytokines and chemokines, as well as the production of reactive oxygen species (ROS), in our EAE model were both suppressed by the KD.
Collectively, our findings indicate that brain inflammation in EAE mice is associated with impaired spatial learning and memory function, and that KD treatment can exert protective effects, likely via attenuation of the robust immune response and increased oxidative stress seen in these animals.