Interruption of β-Catenin Signaling Reduces Neurogenesis in Alzheimer's Disease

• Published in: The Journal of neuroscience Vol. 29; no. 20; pp. 6545 - 6557
• Main Authors: He, Ping, Shen, Yong
• Format: Journal Article
• Language: English
• Published: United States Society for Neuroscience 20.05.2009
• Subjects: Adult Stem Cells - physiology; Age Factors; Aged, 80 and over; Alzheimer Disease - pathology; Alzheimer Disease - physiopathology; Amyloid beta-Peptides - metabolism; Amyloid beta-Peptides - pharmacology; Amyloid beta-Protein Precursor - genetics; Animals; Apoptosis - drug effects; beta Catenin - metabolism; Cells, Cultured; Cerebral Cortex - pathology; Cerebral Cortex - physiopathology; Chondroitin Sulfate Proteoglycans - metabolism; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay - methods; Female; Gene Expression Regulation - physiology; Glycogen Synthase Kinase 3 - genetics; Glycogen Synthase Kinase 3 - metabolism; Glycogen Synthase Kinase 3 beta; Humans; In Situ Nick-End Labeling - methods; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Mutant Proteins - genetics; Nerve Tissue Proteins - metabolism; Neural Cell Adhesion Molecule L1 - metabolism; Neurogenesis - physiology; Neuroglia - drug effects; Neuroglia - metabolism; Neuroglia - pathology; O Antigens - metabolism; Peptide Fragments - metabolism; Peptide Fragments - pharmacology; RNA, Small Interfering - metabolism; Sialic Acids - metabolism; Signal Transduction - physiology; Transfection - methods

The neuronal loss associated with Alzheimer's disease (AD) affects areas of the brain that are vital to cognition. Although recent studies have shown that new neurons can be generated from progenitor cells in the neocortices of healthy adults, the neurogenic potential of the stem/progenitor cel...