Behavior of neural stem cells in the Alzheimer brain

• Published in: Cellular and molecular life sciences : CMLS Vol. 65; no. 15; pp. 2372 - 2384
• Main Authors: Waldau, B, Shetty, A. K
• Format: Journal Article
• Language: English
• Published: Basel Basel : SP Birkhäuser Verlag Basel 01.08.2008; SP Birkhäuser Verlag Basel; Springer Nature B.V
• Subjects: Alzheimer disease; Alzheimer Disease - pathology; Alzheimer's disease; Alzheimer's pathology; Amyloid beta-Peptides - chemistry; Amyloid beta-Peptides - metabolism; Animals; Biochemistry; Biomedical and Life Sciences; Biomedicine; Brain; Brain - pathology; Cell Biology; Cell Differentiation; dentate neurogenesis; Humans; Life Sciences; neural progenitor; neural stem cell; Neurons; Neurons - pathology; Review; stem cell differentiation; stem cell graft; stem cell renewal; Stem cells; Stem Cells - pathology; Studies; stem cell graft; neural stem cell; stem cell renewal; stem cell differentiation; Alzheimer’s disease; neural progenitor; Alzheimer’s pathology; dentate neurogenesis
• ISSN: 1420-682X; 1420-9071
• DOI: 10.1007/s00018-008-8053-y

Alzheimer's disease (AD) is characterized by the deposition of β-amyloid peptides (Aβ) and a progressive loss of neurons leading to dementia. Because hippocampal neurogenesis is linked to functions such as learning, memory and mood, there has been great interest in examining the effects of AD on hippocampal neurogenesis. This article reviews the pertinent studies and tries to unite them in one possible disease model. Early in the disease, oligomeric Aβ may transiently promote the generation of immature neurons from neural stem cells (NSCs). However, reduced concentrations of multiple neurotrophic factors and higher levels of fibroblast growth factor-2 seem to induce a developmental arrest of newly generated neurons. Furthermore, fibrillary Aβ and down-regulation of oligodendrocyte-lineage transcription factor-2 (OLIG2) may cause the death of these nonfunctional neurons. Therefore, altering the brain microenvironment for fostering apt maturation of graft-derived neurons may be critical for improving the efficacy of NSC transplantation therapy for AD.