NGFN-PLUS
Neurological Screen
| Coordinator: | Prof. Dr. Thomas Klopstock | |
| Institution: | Friedrich-Baur-Institut, Neurologische Klinik der LMU | |
| Homepage: | www.baur-institut.de/forschung |
According to a report of the World Health Organization, neurological disorders such as migraine, stroke, Parkinson's disease and dementia affect up to 1 billion people worldwide. The neurological screen focuses on the characterization of mouse models relevant to human neurological diseases to increase knowledge on pathomechanisms and genotype-phenotype relations. Our comprehensive standardized primary screen gives an overall picture of basic neurological functions comparable to what is carried out in human patients. We look for activity, muscle function and coordination of movements, in different paradigms from simple to more complex.
Our main research interests are neurodegeneration and aging as well as mitochondrial diseases as a tool to mimic the alteration in cellular metabolism that is also associated with the age-related decline of neurological functions. Additionally, we are working on dissecting the contribution of environmental factors on disease onset and progression. We analyzed more than 200 lines so far and were able to detect relevant differences in a pleithora of lines, thus contributing to understanding pathomechanisms which will support therapeutic approaches in the future.
In a model for neuronal ceroid lipofuscinosis we detected for example early changes in motor coordination preceding the ones known before. This will support better diagnosis and further reseach of the fatal human disease. In another mutant we closely analysed a mouse line with a mutation in a structural mitochondrial protein. The impaired motor coordination, posture and muscle strength reduction found in our analysis sheds new light on the observed gene activity differences in diseases like Huntington, Parkinson and ALS.
Moreover appropriate mouse models (e.g. for neurodegenerative diseases) are used for therapeutic and neuroprotective trials. In one study we supplemented aging mice with creatine and could show that not only life expectancy was increased but also cognitive functions improved, supporting the neuroprotective effects of creatine.
Additional relevant Internet links:
The German Mouse Clinic
Further Coordinators:
Our main research interests are neurodegeneration and aging as well as mitochondrial diseases as a tool to mimic the alteration in cellular metabolism that is also associated with the age-related decline of neurological functions. Additionally, we are working on dissecting the contribution of environmental factors on disease onset and progression. We analyzed more than 200 lines so far and were able to detect relevant differences in a pleithora of lines, thus contributing to understanding pathomechanisms which will support therapeutic approaches in the future.
In a model for neuronal ceroid lipofuscinosis we detected for example early changes in motor coordination preceding the ones known before. This will support better diagnosis and further reseach of the fatal human disease. In another mutant we closely analysed a mouse line with a mutation in a structural mitochondrial protein. The impaired motor coordination, posture and muscle strength reduction found in our analysis sheds new light on the observed gene activity differences in diseases like Huntington, Parkinson and ALS.
Moreover appropriate mouse models (e.g. for neurodegenerative diseases) are used for therapeutic and neuroprotective trials. In one study we supplemented aging mice with creatine and could show that not only life expectancy was increased but also cognitive functions improved, supporting the neuroprotective effects of creatine.
Additional relevant Internet links:
The German Mouse Clinic
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