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Prove of the maternal influence for the development of Alzheimers disease26.04.2012 - (idw) Universitätsklinikum Magdeburg
Neurodegenerative disorders with dementia play an increasing role in the aging western population, esp. for the care and health systems. In 2050, an estimated number of 106-360 million demented patients have to be taken care of. Alzheimers disease comprises 2/3 of all dementia cases. It is an age-related disease that starts to effect patients in their 60ies and older. Only less than 1% are hereditary cases where specific mutations are known. Till now, age is the most important risk factor for sporadic Alzheimers disease with the risk being even more elevated if the mother or the grandmother were sufferers.
The research team led by Jens Pahnke (M.D., Ph.D., E.F.N.) from the University of Magdeburg (Germany) discovered an important link between maternal inheritance and the deposition of toxic amyloid in Alzheimers disease. They established new mouse models that mimic the maternal inheritance of mitochondria. In an international collaboration with colleagues from the USA, Canada, France and Germany they discovered that increased activity of mitochondria leads to a reduced deposition rate of the toxic Alzheimer peptides. In mice with the highest mitochondrial activity they discovered an approximately 80% reduction of amyloid as compared to mice with mitochondria that exhibited much lower activity. In October 2011, they discovered a new Alzheimers gene that also directly depends on the cellular energy produced by the mitochondria. Now they link these new findings to explain age related changes, maternal inheritance and impairment of toxic amyloid export from the brain.
Interestingly, the mental capacity of the brain is directly linked to the availability of energy as produced by mitochondria. It has long been discussed why high education and rate of disease are inversely correlated. The different activities of mitochondria may provide a tool to explain the latter fact.
Artikel/article online 0:23, 21.Apr.2012 in Acta Neuropathologica
Jens Pahnke, Universität Magdeburg, Neurodegeneration Research Lab (NRL), Leipziger Str 44, 39120 Magdeburg, Germany, Tel: +49 391 67 24514, Email: email@example.com
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