BACKGROUND: The causes of Amyotrophic Lateral Sclerosis (ALS) are unknown. A bulk of evidence supports the hypothesis that oxidative stress and mitochondrial dysfunction can be implicated in ALS pathogenesis. METHODS =: We assessed, in cerebrospinal fluid (CSF) and in plasma of 49 ALS patients and 8 controls, the amount of oxidized proteins (AOPP, advanced oxidation protein products), the total antioxidant capacity (FRA, the ferric reducing ability), and, in CSF, two oxidation products, the 4-hydroxynonenal and the sum of nitrites plus nitrates. RESULTS: The FRA was decreased (p = 0.003) in CSF, and AOPP were increased in both CSF (p = 0.0039) and plasma (p = 0.001) of ALS patients. The content of AOPP was differently represented in CSF of ALS clinical subsets, resulting in increase in the common and pseudopolyneuropathic forms (p < 0.001) and nearly undetectable in the bulbar form, as in controls. The sum of nitrites plus nitrates and 4-hydroxynonenal were unchanged in ALS patients compared with controls. CONCLUSION: Our results, while confirming the occurrence of oxidative stress in ALS, indicate how its effects can be stratified and therefore implicated differently in the pathogenesis of different clinical forms of ALS.
BACKGROUND: The causes of Amyotrophic Lateral Sclerosis (ALS) are unknown. A bulk of evidence supports the hypothesis that oxidative stress and mitochondrial dysfunction can be implicated in ALS pathogenesis. METHODS =: We assessed, in cerebrospinal fluid (CSF) and in plasma of 49 ALS patients and 8 controls, the amount of oxidized proteins (AOPP, advanced oxidation protein products), the total antioxidant capacity (FRA, the ferric reducing ability), and, in CSF, two oxidation products, the 4-hydroxynonenal and the sum of nitrites plus nitrates. RESULTS: The FRA was decreased (p = 0.003) in CSF, and AOPP were increased in both CSF (p = 0.0039) and plasma (p = 0.001) of ALS patients. The content of AOPP was differently represented in CSF of ALS clinical subsets, resulting in increase in the common and pseudopolyneuropathic forms (p < 0.001) and nearly undetectable in the bulbar form, as in controls. The sum of nitrites plus nitrates and 4-hydroxynonenal were unchanged in ALS patients compared with controls. CONCLUSION: Our results, while confirming the occurrence of oxidative stress in ALS, indicate how its effects can be stratified and therefore implicated differently in the pathogenesis of different clinical forms of ALS.
Authors: M Cosottini; G Donatelli; M Costagli; E Caldarazzo Ienco; D Frosini; I Pesaresi; L Biagi; G Siciliano; M Tosetti Journal: AJNR Am J Neuroradiol Date: 2015-12-17 Impact factor: 3.825
Authors: D Allan Butterfield; Marzia Perluigi; Tanea Reed; Tasneem Muharib; Christopher P Hughes; Renã A S Robinson; Rukhsana Sultana Journal: Antioxid Redox Signal Date: 2012-01-18 Impact factor: 8.401
Authors: Katharine Nicholson; James Chan; Eric A Macklin; Mark Levine-Weinberg; Christopher Breen; Rachit Bakshi; Daniela L Grasso; Anne-Marie Wills; Samad Jahandideh; Albert A Taylor; Danielle Beaulieu; David L Ennist; Ovidiu Andronesi; Eva-Maria Ratai; Michael A Schwarzschild; Merit Cudkowicz; Sabrina Paganoni Journal: Ann Clin Transl Neurol Date: 2018-10-22 Impact factor: 4.511
Authors: Nick S Verber; Stephanie R Shepheard; Matilde Sassani; Harry E McDonough; Sophie A Moore; James J P Alix; Iain D Wilkinson; Tom M Jenkins; Pamela J Shaw Journal: Front Neurol Date: 2019-04-03 Impact factor: 4.003