By a News Reporter-Staff News Editor at Gene Therapy Weekly -- Fresh data on Biotechnology are presented in a new report. According to news reporting from San Diego, California, by NewsRx journalists, research stated, "Brain-derived neurotrophic factor (BDNF) improves molecular, cellular, and behavioral measures of neural dysfunction in genetic models of Alzheimer's disease (Blurton-Jones et al., 2009; Nagahara et al., 2009). However, BDNF treatment after disease onset has not been reported to improve neuronal survival in these models."
The news correspondents obtained a quote from the research from Veterans Affairs Medical Center, "We now report prevention of neuronal loss with early life BDNF treatment in mutant mice expressing two amyloid precursor protein (APP) mutations associated with early-onset familial Alzheimer's disease. APP transgenic mice underwent lentiviral BDNF gene delivery into the entorhinal cortices at age 2 months and were examined 5 months later. BDNF-treated mice exhibited significant improvements in hippocampal-dependent contextual fear conditioning compared with controltreated APP mice (p < 0.05). Stereological analysis of entorhinal cortical cell number demonstrated similar to 20% reductions in neuronal number in layers II-VI of the entorhinal cortex in untreated APP mutant mice compared with wild-type mice (p < 0.0001), and significant amelioration of cell loss by BDNF (p < 0.001). Moreover, BDNF gene delivery improved synaptophysin immunoreactivity in the entorhinal cortex and, through anterograde BDNF transport, in the hippocampus (p < 0.01)."
According to the news reporters, the research concluded: "Notably, BDNF did not affect amyloid plaque numbers, indicating that direct amyloid reduction is not necessary to achieve significant neuroprotective benefits in mutant amyloid models of Alzheimer's disease."
For more information on this research see: Early BDNF Treatment Ameliorates Cell Loss in the Entorhinal Cortex of APP Transgenic Mice. Journal of Neuroscience, 2013;33(39):15596-15602. Journal of Neuroscience can be contacted at: Soc Neuroscience, 11 Dupont Circle, NW, Ste 500, Washington, DC 20036, USA. (Society for Neuroscience - www.sfn.org/; Journal of Neuroscience - www.sfn.org/index.aspx?pagename=JournalOfNeuroscience)
Our news journalists report that additional information may be obtained by contacting A.H. Nagahara, Vet Affairs Med Center, San Diego, CA 92161, United States. Additional authors for this research include M. Mateling, I. Kovacs, L. Wang, S. Eggert, E. Rockenstein, E.H. Koo, E. Masliah and M.H. Tuszynski (see also technology.html">Biotechnology).
Keywords for this news article include: Biotechnology, Cells, Amyloid, Neurons, Cerebrum, Dementia, Proteins, San Diego, Treatment, California, Tauopathies, Gene Therapy, United States, Telencephalon, Bioengineering, Brain Diseases, Cerebral Cortex, Alzheimer Disease, Entorhinal Cortex, Parahippocampal Gyrus, North and Central America, Neurodegenerative Diseases
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