Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease resulting from loss of upper and lower motor neurons. Although the majority of ALS cases are sporadic, 5–10% of patients have a positive family history. The pivotal histopathological finding of sporadic ALS is intraneuronal aggregates of TDP-43. Recent advancement in genetics identified a variety genetic cause of ALS, including C9orf72, TDP-43, FUS and SOD1. This provides a tight link between this disease and frontotemporal lobar degeneration (FTLD) as well as important molecular insight into ALS/FTLD such as dysregulated RNA metabolism, disrupted protein quality control, axonal transport impairment and nuclear transport deficit, among others. In this symposium, cutting-edge research on the pathogenesis and therapy development for ALS and related disorders will be discussed.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease resulting from loss of upper and lower motor neurons. Although the majority of ALS cases are sporadic, 5–10% of patients have a positive family history. The pivotal histopathological finding of sporadic ALS is intraneuronal aggregates of TDP-43. Recent advancement in genetics identified a variety genetic cause of ALS, including C9orf72, TDP-43, FUS and SOD1. This provides a tight link between this disease and frontotemporal lobar degeneration (FTLD) as well as important molecular insight into ALS/FTLD such as dysregulated RNA metabolism, disrupted protein quality control, axonal transport impairment and nuclear transport deficit, among others. In this symposium, cutting-edge research on the pathogenesis and therapy development for ALS and related disorders will be discussed.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease resulting from loss of upper and lower motor neurons. Although the majority of ALS cases are sporadic, 5–10% of patients have a positive family history. The pivotal histopathological finding of sporadic ALS is intraneuronal aggregates of TDP-43. Recent advancement in genetics identified a variety genetic cause of ALS, including C9orf72, TDP-43, FUS and SOD1. This provides a tight link between this disease and frontotemporal lobar degeneration (FTLD) as well as important molecular insight into ALS/FTLD such as dysregulated RNA metabolism, disrupted protein quality control, axonal transport impairment and nuclear transport deficit, among others. In this symposium, cutting-edge research on the pathogenesis and therapy development for ALS and related disorders will be discussed.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease resulting from loss of upper and lower motor neurons. Although the majority of ALS cases are sporadic, 5–10% of patients have a positive family history. The pivotal histopathological finding of sporadic ALS is intraneuronal aggregates of TDP-43. Recent advancement in genetics identified a variety genetic cause of ALS, including C9orf72, TDP-43, FUS and SOD1. This provides a tight link between this disease and frontotemporal lobar degeneration (FTLD) as well as important molecular insight into ALS/FTLD such as dysregulated RNA metabolism, disrupted protein quality control, axonal transport impairment and nuclear transport deficit, among others. In this symposium, cutting-edge research on the pathogenesis and therapy development for ALS and related disorders will be discussed.