The Laboratory for Molecular Neuroscience investigates molecular mechanisms involved in the development of acute and chronic neurodegenerative disease, with a focus on the role of glutamate excitotoxicity. It aims at unraveling the molecular basis for cell death and edema development in stroke, and explores the pathophysiology of Alzheimer''s disease and temporal lobe epilepsy. One of the long term goals is to identify new molecular targets for neuroprotective strategies in stroke and other conditions involving glutamate excitotoxicity. The main objective of the LMN is to advance our understanding of the role of glutamate, as a transmitter substance in the normal brain and as a mediator of excitotoxicity in pathological conditions such as stroke. To this end the LMN employs several vital and non-vital imaging techniques. Model systems include organotypical slice cultures and transgene animals. It is believed that the excitotoxic cascade ultimately leads to DNA damage, partly through excessive formation of oxygen radicals. Thus an important focus of the LMN is to explore the role of DNA damage and repair in the pathogenesis of neurodegenerative disease. LMN is also engaged in research on molecular mechanism underlying brain edema, epilepsy, and Alzheimer''s disease. Clinical perspective of LMN''s activities The field of neurology continues to lag behind those of other disciplines when it comes to the range and efficacy of therapeutic strategies. In particular, common neurological conditions such as stroke, Alzheimer''s disease, Parkinson''s disease and other chronic neurodegenerative diseases, age-related cognitive impairment, epilepsy, mood disorders and schizophrenia call for new therapeutic strategies. Several of these conditions are particularly prevalent among the elderly and will constitute a growing health concern as the population ages. Most of the current molecular targets for neurological therapy are found in the monoamine and acetylcholine signaling systems, as use of receptor blockers or other drugs to interfere with the widespread fast signal transmission systems are causing substantial side effects. Future therapies will have to be based on strategies that act by reducing or increasing the number or activity of specific subtypes of pre- and postsynaptic receptors, transporters, and ion channels, or other membrane molecules at the synapse, and by strategies that exploit the new possibilities offered by stem cell technology and targeted repair.
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epilepsy, excitotoxicity, acute, alzheimer''s disease, brain, brain edema, cell death, chronic, damage, dna, glutamate, imaging, model systems, molecular, molecular mechanisms, neurodegenerative disease, neuroprotective, neuroscience, normal, repair, stroke, transmitter
University of Oslo LMN
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