Abstract

Motor neuron disease (MND) is a terrible neurodegenerative illness with a poor prognosis and significant impairment. Despite recent advances in symptomatic care, there are few medicines that can affect survival. However, a better understanding of the underlying etiology would substantially aid the task of finding effective treatments. In the etiology of MND, many potential external risk factors have been hypothesized as part of a gene-environment interaction. Following reports of a greater than predicted incidence of MND in professional athletes, there has been an increasing interest in the role of intensive physical exercise in the development of the disease. Current hypotheses about the cellular and genetic causes of MND also support this conclusion. Epidemiological evidence, on the other hand, is contradictory and inconclusive. FTD/motor neuron disease is the name given to a motor neuronopathy that complicates frontotemporal dementia (FTD) (MND). FTD is marked by severe personality changes, abnormal social behavior, and executive difficulties caused by frontal and temporal neocortical atrophy. Bulbar palsy and limb amyotrophy are symptoms of motor neuron disease. Micro vacuolation of the cerebral cortex is the most common histological alteration, along with atrophy of the bulbar neurons and anterior horn cells of the spinal cord. Large pyramidal cortical neurons, surviving cranial nerve nuclei, and anterior horn cells all have ubiquitinated inclusion bodies. Evidence is accumulating that some patients with classical MND/amyotrophic lateral sclerosis (ALS) who are not regarded to be demented show frontal executive function abnormalities. Moreover, frontal lobe abnormalities have been demonstrated by neuroimaging. Keywords: MND, FTD, ALS, motor neuron, behavior, physical activity, cognitive change.

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