Vol 2-4 Commentary

Commentary: Calcium in the pathomechanism of amyotrophic lateral sclerosis - Taking center stage?

Valéria Meszlényi1, Roland Patai2, Bernát Nógrádi1, József I. Engelhardt3, László Siklós2

1Foundation for the Future of Biomedical Sciences in Szeged, Pálfy u. 52/d, H-6725 Szeged, Hungary

2Institute of Biophysics, Biological Research Center of the Hungarian Academy of Sciences, Temesvári krt. 62, H-6726 Szeged, Hungary

3Department of Neurology, University of Szeged, Semmelweis u. 6, H-6725 Szeged, Hungary

 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.

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Vol 2-4 Commentary

Commentary: Case-based learning and multiple choice questioning methods favored by students

Magalie Chéron1 and Henriette Löffler-Stastka1*

1Department for Psychoanalysis and Psychotherapy, Advanced Postgraduate Program for Psychotherapy Research, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria

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Vol 2-4 Mini Review

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*

1Psychopathology and Cognitive Neuropsychology Unit, Faculty of Psychology and Educational Sciences, University of Geneva, Boulevard du Pont d’Arve 40, CH-1205 Geneva, Switzerland

2Consultation Vieillir et Bien Vivre, Clinique et Permanence d’Onex, Cité Générations, Route de Chancy 98, CH-1213 Onex, Switerland

3Swiss Center for Affective Sciences, Campus Biotech, University of Geneva, Case Postale 60, CH-1211 Geneva, Switzerland

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.

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