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LIN: Forschungsabteilungen > Akkustik, Lernen, Sprache > Unterpunkt Ebene 3 > Unterpunkt Ebene 4
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LIN: Forschungsabteilungen > Akkustik, Lernen, Sprache > Unterpunkt Ebene 3 > Unterpunkt Ebene 4
Titel: LIN Layout
Head:Prof. Dr. Klaus G. ReymannProject Group Neuropharmacology Leibniz Institute for Neurobiology Brenneckestraße 6 39118 Magdeburg Germany
The research of our Project group Neuropharmacology is focused on the pathophysiology and pharmacology of cerebral ischemia and Alzheimer dementia. Some of our ongoing projects are realized in close collaboration with the DZNE Magdeburg and the Research Institute for Applied Neurosciences (FAN gGmbH). An ischemic insult is the result of an
insufficient blood flow within the brain, followed by failures of function,
disability and dementia. Thus, it is a prevalent disease and also the
third-most reason for death. To date, there is no common pharmacological
neuroprotection after an ischemic insult in clinics. So far the only reliable
therapy after stroke is thrombolysis in specific patients. Thus, there is a
huge importance to improve motor skills and cognitive functionality after an
insult. During the last decade the literature has shown that even in the adult
brain a formation of new neurons can occur. We focus on possible regeneration
after an ischemic insult, based on proliferation, migration and functional
integration of endogenous stem cells as well as transplanted adult stem cells. We investigate the post-ischemic
mechanisms of regeneration and neuronal plasticity in rodent tissue cultures
and in behavioral models. Post-stroke events also include an inflammatory
reaction of the brain and the periphery. Recently, we could identify a new
neuroprotective mechanisms of the CNS whereby microglia (the brain macrophages) guards neurons by the engulfment
of toxic neutrophil granulocytes and direct cell-cell contacts between
microglia and neurons in an in vitro stroke model. The increased life expectancy of people in industrialized nations is linked to a rise in age-related illnesses, most notably neurodegenerative diseases such as Alzheimer's dementia. The disturbances of neuronal function induced by sublethal Abeta concentrations are hypothesized to be the first stages of the cognitive decline in patients. It is known that Abeta oligomerization leads to the impairment of long-term potentiation, a form of synaptic memory. With electrophysiological techniques in hippocampal slices we investigate the mechanisms and related drug targets of amyloid beta-induced functional disturbances testing synaptic plasticity (long term potentiation-LTP). Annual Report:
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