Amyotrophic Lateral Sclerosis (ALS) etiology and pathogenesis still remain elusive. However, several genetic and environmental factors have been suggested to play a role in the genesis of the disease.
Among these, some metabolic disturbances such as dyslipidemia, diabetes, and urate were found to have different frequencies among ALS patients and matched controls. It was also reported that some patients show an increased resting energy expenditure that also affects the disease prognosis.
Together with evidence supporting the involvement of multiple systems (cognition and also the extrapyramidal system and autonomous nervous system), data on the contribution of metabolic alterations to the disease reinforce the idea that ALS is not simply a motor disease but rather is a multi-systemic syndrome.
Dyslipidemia, for example, is now recognized as a bona fide risk factor for ALS. It has been evaluated using various measures (LDL, LDL/HDL ratio, apolipoproteins) and despite being prone to many possible confounders (such as other cardiovascular risk factors or socio-economical status), genetic studies confirmed its role in the pathogenesis of the disease. Contrarily, diabetes and other cardiovascular risk factors are usually inversely correlated with ALS risk. Urate blood levels are usually higher among ALS patients.
Interestingly, dyslipidemia could have an inverse effect on prognosis, being associated with a longer survival. Diabetes does not seem to influence the disease progression.
It is therefore necessary to evaluate how future directions and studies might help understand the causes and consequences of metabolic dysfunctions impacting neurodegeneration and provide grounds for new potential treatment strategies.
This Research Topic aims to collect evidence on the presence of metabolic alterations and their frequency in ALS, focusing on their risk and prognostic effect and providing grounds to support the multi-systemic nature of ALS.
While some of these studies could be replicative with respect to previous findings, original articles about unexplored aspects of this relationship will be valued. Given the relationship's nature, manuscripts should also consider possible confounders in their analyses (such as other cardiovascular risk factors). Alternatively, manuscripts could provide an updated review on this topic.
To this aim we welcome articles addressing the following, but not limited to, questions:
• unexplored aspects of the role of lipids metabolism in ALS
• new and unexplored metabolic disturbances in ALS
• on the primacy of such alterations: are metabolic dysfunctions pathogenetic or adaptive responses in ALS?
• evidence of intracellular modifications linked to metabolic disturbances in ALS – cellular and animal model studies
• a global view on how different metabolic dysfunctions could be linked together and to the neurodegenerative process in Amyotrophic Lateral Sclerosis
Amyotrophic Lateral Sclerosis (ALS) etiology and pathogenesis still remain elusive. However, several genetic and environmental factors have been suggested to play a role in the genesis of the disease.
Among these, some metabolic disturbances such as dyslipidemia, diabetes, and urate were found to have different frequencies among ALS patients and matched controls. It was also reported that some patients show an increased resting energy expenditure that also affects the disease prognosis.
Together with evidence supporting the involvement of multiple systems (cognition and also the extrapyramidal system and autonomous nervous system), data on the contribution of metabolic alterations to the disease reinforce the idea that ALS is not simply a motor disease but rather is a multi-systemic syndrome.
Dyslipidemia, for example, is now recognized as a bona fide risk factor for ALS. It has been evaluated using various measures (LDL, LDL/HDL ratio, apolipoproteins) and despite being prone to many possible confounders (such as other cardiovascular risk factors or socio-economical status), genetic studies confirmed its role in the pathogenesis of the disease. Contrarily, diabetes and other cardiovascular risk factors are usually inversely correlated with ALS risk. Urate blood levels are usually higher among ALS patients.
Interestingly, dyslipidemia could have an inverse effect on prognosis, being associated with a longer survival. Diabetes does not seem to influence the disease progression.
It is therefore necessary to evaluate how future directions and studies might help understand the causes and consequences of metabolic dysfunctions impacting neurodegeneration and provide grounds for new potential treatment strategies.
This Research Topic aims to collect evidence on the presence of metabolic alterations and their frequency in ALS, focusing on their risk and prognostic effect and providing grounds to support the multi-systemic nature of ALS.
While some of these studies could be replicative with respect to previous findings, original articles about unexplored aspects of this relationship will be valued. Given the relationship's nature, manuscripts should also consider possible confounders in their analyses (such as other cardiovascular risk factors). Alternatively, manuscripts could provide an updated review on this topic.
To this aim we welcome articles addressing the following, but not limited to, questions:
• unexplored aspects of the role of lipids metabolism in ALS
• new and unexplored metabolic disturbances in ALS
• on the primacy of such alterations: are metabolic dysfunctions pathogenetic or adaptive responses in ALS?
• evidence of intracellular modifications linked to metabolic disturbances in ALS – cellular and animal model studies
• a global view on how different metabolic dysfunctions could be linked together and to the neurodegenerative process in Amyotrophic Lateral Sclerosis