Conference Report (8th Annual Meeting of the Society for the Study of Neuroprotection and Neuroplasticity)

Author(s): Stephen D. Skaper.

Journal Name: CNS & Neurological Disorders - Drug Targets
(Formerly Current Drug Targets - CNS & Neurological Disorders)

Volume 11 , Issue 4 , 2012

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Abstract:

The Society for the Study of Neuroprotection and Neuroplasticity (SSNN) was created in 2005 by an international group of clinicians and basic scientists under the initiative of Prof. Dafin F. Muresanu, University of Medicine and Pharmacy “Iuliu Hatieganu”, Cluj-Napoca, Romania. The SSNN is a scientific organization focusing on basic and clinical research, whose goal is to create a discussion platform to facilitate our understanding of endogenous basic biological processes together with the development of pharmacological and non-pharmacological strategies for positive manipulation of neurotrophicity, neuroprotection, neuroplasticity and neurogenesis. The Society subsequently became an affiliated organ of the Global College of Neuroprotection and Neuroregeneration (GCNN), founded in 2004 by Russell Pendleton, London, UK and Hari Shanker Sharma, Uppsala, Sweden.

Dubrovnik, a Croatian city on the suggestive Adriatic Sea coast, and among UNESCO’s list of World Heritage Sites, was the venue for this year’s annual meeting of the SSNN. The themes covered include brain protection and recovery, dementia, neurorehabilitation, and traumatic brain injury.

There is increasing evidence that cerebrovascular dysfunction plays a role in vascular causes of cognitive impairment and also in Alzheimer’s disease. Vascular dementia can be viewed as a heterogeneous cluster of different syndromes and disorders with cognitive deficit, and whose treatment is a challenging issue. Data were presented suggesting that one approach to this problem may be the use of a suitable combination of neurotrophic factors/peptides, in a brain-penetrant form, for example Cerebrolysin (neurotrophic peptidergic mixture produced by standardized enzymatic breakdown of lipid-free porcine brain proteins), which has been documented to attenuate central nervous system pathologies following traumatic or metabolic insults to the brain or spinal cord.

Is “senile dementia of the Alzheimer type” the result of a combination of several processes, operating differently in each individual? It was suggested that perhaps Alzheimer’s disease should more correctly be regarded as a syndrome which can result from many different etiologies, some genetic but mostly environmental (risk factors such as hypertension, hypercholesterolemia, metabolic disease, smoking, and obesity). As such, combating dementia should begin in midlife, not in old age.

Neurorehabilitation is a speciality of neuroscience, which deals with the study and application of complex medical processes aiming at recovery from nervous system injury and to compensate for functional alterations. Beside the use of training techniques and other behavioral interventions, neurological rehabilitation can be promoted by the use of pharmacological agents. In addition to pharmacological treatments for risk factors such as hypertension and hyperlipidemia and secondary prevention, drugs can also be used to facilitate brain recovery. The utilization of particular drugs for neuroprotection and brain repair was discussed, along with the concept of mono- vs multimodal action. Positive data from a recent multicenter stroke trial with Cerebrolysin were also presented.

Traumatic brain injury (TBI), also known as intracranial injury, occurs when an external force traumatically injures the brain. TBI is a major cause of death and disability worldwide, especially in children and young adults. In addition to the damage caused at the moment of injury, brain trauma causes secondary injury, a variety of events that take place in the minutes and days following the injury. These processes, which include alterations in cerebral blood flow and pressure within the skull, contribute substantially to damage from the initial injury. An important diagnostic aspect of TBI today includes imaging techniques such as computed tomography and magnetic resonance imaging; for the latter, novel methods to measure cerebrovascular reactivity non-invasively show promise for identifying vascular endophenotypes in TBI. Diffusion Tensor Imaging shows encouraging development as a tool to measure diffuse axonal injury, which is a prominent mechanism of TBI. Up-and-coming quantitative volumetric methods allow detection of regional changes in brain structure after TBI, and identify brain regions which are particularly susceptible to diffuse traumatic insults. Depending on the injury, treatment required may be minimal or may include interventions such as medications and emergency surgery. Approaches to restorative treatment in experimental models of TBI were discussed, including the use of cell-based therapy, and pharmacological therapies comprising erythropoietin, statins, Thymosin B4 and Cerebrolysin. These treatments promote brain remodeling and thereby enhance neurological and cognitive outcomes. Moreover, magnetic resonance imaging can be used as an index to monitor restorative response.

Contrary to what was once believed, we are now coming to appreciate that nervous system repair and neurorestoration is an accomplishable goal.

To paraphrase the English biologist Thomas Henry Huxley (1825 - 1895): “The great tragedy of science - the slaying of a beautiful hypothesis by an ugly fact.”

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Article Details

VOLUME: 11
ISSUE: 4
Year: 2012
Page: [333 - 334]
Pages: 2
DOI: 10.2174/187152712800792802

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