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• W2020935865 abstract "Amyotrophic lateral sclerosis (ALS) is a relentless fatal paralytic disorder confined to the voluntary motor system (1). Its prevalence is about three to five in 100,000 individuals, making it the most frequent paralytic disease in adults. Although ALS can strike anyone at any age, generally the onset of the disease is in the fourth or fifth decade of life. Common clinical features of ALS include muscle weakness, fasciculations, brisk (or depressed) reflexes, and extensor plantar responses. Even though motor deficit usually predominates in the limbs, bulbar enervation can also be severely affected, leading to atrophy of the tongue, dysphagia, and dysarthria. Other cranial nerves (e.g., oculomotor nerves) are usually spared. The progressive decline of muscular function results in paralysis, speech and swallowing disabilities, emotional disturbance, and, ultimately, respiratory failure causing death among the vast majority of ALS patients within 2–5 years after the onset of the disease. Pathologically, ALS is characterized by a loss of upper motor neurons in the cerebral cortex and of the lower motor neurons in the spinal cord. Often, there is also a profound degeneration of the corticospinal tracts, which is most evident at the level of the spinal cord. The few remaining motor neurons are generally atrophic, and many demonstrate abnormal accumulation of neurofilament, in both their cell bodies and axons. To date, only a few approved treatments (e.g., mechanical ventilation and riluzole) prolong survival in ALS patients to some extent. However, the development of more effective neuroprotective therapies remains impeded by our limited knowledge of the actual mechanisms by which neurons die in ALS, and of how the disease progresses and propagates.ALS, like other common neurodegenerative disorders, is sporadic in the vast majority of patients, and familial in only a few (1). The clinical and pathological expressions of ALS are almost indistinguishable between the familial and sporadic forms, although often in the former the age at onset is younger, the course of the disease more rapid, and the survival after diagnosis shorter (1). The cause of sporadic ALS remains unknown, while that of at least some familial forms has been identified (see below). Although the identified gene defects responsible for ALS account for a minute fraction of cases, most experts believe that unraveling the molecular basis by which those mutant gene products cause neurodegeneration may shed light on the etiopathogenesis of the common sporadic form of ALS." @default.
• W2020935865 created "2016-06-24" @default.
• W2020935865 creator A5008653620 @default.
• W2020935865 creator A5057571524 @default.
• W2020935865 date "2003-01-15" @default.
• W2020935865 modified "2023-09-23" @default.
• W2020935865 title "Programmed cell death in amyotrophic lateral sclerosis" @default.
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• W2020935865 doi "https://doi.org/10.1172/jci17610" @default.
• W2020935865 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/151885" @default.
• W2020935865 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12531867" @default.
• W2020935865 hasPublicationYear "2003" @default.
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