Imbalance of p75(NTR)/TrkB protein expression in Huntington's disease: implication for neuroprotective therapies

• Published in: Cell death & disease Vol. 4; p. e595
• Main Authors: Brito, V, Puigdellívol, M, Giralt, A, del Toro, D, Alberch, J, Ginés, S
• Format: Journal Article
• Language: English
• Published: England 18.04.2013
• Subjects: Animals; Apoptosis - drug effects; Brain-Derived Neurotrophic Factor - pharmacology; Brain-Derived Neurotrophic Factor - therapeutic use; Cell Line; Corpus Striatum - metabolism; Disease Models, Animal; Enzyme Inhibitors - pharmacology; Gene Knock-In Techniques; Humans; Huntington Disease - drug therapy; Huntington Disease - metabolism; Huntington Disease - pathology; JNK Mitogen-Activated Protein Kinases - metabolism; Mice; N-Methylaspartate - pharmacology; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - metabolism; Nuclear Proteins - genetics; Nuclear Proteins - metabolism; Okadaic Acid - pharmacology; Phosphorylation; Protein Binding; Protein Phosphatase 1 - antagonists & inhibitors; Protein Phosphatase 1 - metabolism; Proto-Oncogene Proteins c-akt - metabolism; Putamen - metabolism; Receptor, Nerve Growth Factor - antagonists & inhibitors; Receptor, Nerve Growth Factor - genetics; Receptor, Nerve Growth Factor - metabolism; Receptor, trkB - metabolism; RNA Interference; RNA, Small Interfering - metabolism; Signal Transduction

Neuroprotective therapies based on brain-derived neurotrophic factor (BDNF) administration have been proposed for Huntington's disease (HD) treatment. However, our group has recently reported reduced levels of TrkB in HD mouse models and HD human brain suggesting that besides a decrease on BDNF...