Commentary: Calcium in the pathomechanism of amyotrophic lateral sclerosis - Taking center stage?
Valéria Meszlényi1, Roland Patai2, Bernát Nógrádi1, József I. Engelhardt3, László Siklós2
Amyotrophic lateral sclerosis is a rare and fatal neurodegenerative disorder characterized by the progressive loss of motor neurons in the central nervous system and neuromuscular junctions in the periphery. The pathomechanism behind the disease, except from some familiar cases associated with genetic mutations, remains unclear, however, numerous mechanisms contributing to the disease have already been disclosed. The key components are the oxidative stress, excitotoxicity, mitochondrial dysfunctions and inflammatory processes. In addition, increased intracellular calcium, which is another identified pathological event, could merge these individual toxic mechanisms into a single, escalating and self-perpetuating cycle of neuronal degeneration. Our previous results suggest that calcium homeostasis might be preserved by modulating the transmembrane calcium flux with therapeutic compounds or via altering the calcium binding protein content to maintain an enhanced calcium buffer capacity. The scope of this commentary is to accentuate the reciprocal calcium dependence of the pathological events associated with amyotrophic lateral sclerosis and to discuss possible therapeutic strategies based on the restoration of calcium homeostasis.
DOI: 10.29245/2572.942X/2017/4.1123 View / Download Pdf Commentary: Case-based learning and multiple choice questioning methods favored by students
DOI: 10.29245/2572.942X/2017/4.1126 View / Download PdfMagalie Chéron1 and Henriette Löffler-Stastka1*
A life-span and plurifactorial view of Alzheimer's disease
Julien Leblond1, Anne-Claude Juillerat Van der Linden1,2, and Martial Van der Linden1,3*
The dominant biomedical position considers Alzheimer’s disease (AD) to be intrinsically different from normal ageing and other neurodegenerative diseases and proposes that, by pursuing extensive research on what are considered the specific neuropathological characteristics of AD (i.e., neurotic plaques and neurofibrillary tangles), we will eventually be able to identify the cause of this disease and develop medical treatments that will allow us to successfully cure it. However, results of numerous recent studies go against this essentialist and category-based view and instead suggest that the cognitive, emotional, behavioural, and functional difficulties that some people experience as they grow older are modulated by a myriad of factors and mechanisms that interact throughout the lifespan. Importantly, this alternative way of conceptualising Alzheimer’s disease implies a shift of focus in terms of research objectives and calls for significant changes in terms of neuropsychological assessment and intervention in clinical practice.
DOI: 10.29245/2572.942X/2017/4.1121 View / Download Pdf