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Clinical Neuroscience

JULY 30, 2017

[Calcium ion is a common denominator in the pathophysiological processes of amyotrophic lateral sclerosis]

PATAI Roland, NÓGRÁDI Bernát, MESZLÉNYI Valéria, OBÁL Izabella, ENGELHARDT József István, SIKLÓS László

[Amyotrophic lateral sclerosis (ALS), the most frequent motor neuron disease is characterized by progressive muscle weakness caused by the degeneration of the motor neurons in the spinal cord and motor cortex. However, according to the recent observations, ALS is a rather complex syndrome which frequently involves symptoms of cognitive impairment. Therefore, ALS cases can be interpreted in a clinico-pathological spectrum spanning from the classical ALS involving only the motor system to the fronto-temporal dementia. The progression of the disease, however, manifested in the degeneration of the upper and lower motor neurons, is based on the same complex pathobiology. The main elements of the pathomechanism, such as oxidative stress, excitotoxicity, immune/inflammatory processes and mitochondrial dysfunction are well described already, which operate in orchestrated way and amplify the deleterious effect of each other. It is assumed that calcium ions act as a catalyst in this interaction, hence each of the individual mechanisms has strong, positive and reciprocal calcium dependence thus may combine the individual pathological processes into a unified escalating mechanism of neuronal destruction. This review provides an overview of the role of calcium in connecting and amplifying the major mechanisms which lead to degeneration of the motor neurons in ALS. ]

Clinical Neuroscience

JANUARY 20, 2009

[Neuroprotection in Parkinson’s disease and other neurodegenerative disorders: preclinical and clinical findings]


[The authors summarized the evidence supporting neuroprotection based on the data available in the literature. In vivo and in vitro studies have indicated that many compounds can decrease neurodegeneration, excitotoxicity, oxidative stress, protein aggregation, disturbance of Ca2+ homeostasis and compensate the energy impairment. Selegiline, rasagiline, dopamine agonists and other molecules (ubiquinone, kynurenic acid, tocopherol, creatine, glatiramer acetate) exert neuroprotective effects in preclinical studies. Much less clinical data are available regarding neuroprotection in different neurological disorders. In this review, such preclinical and clinical evidences are summarized.]