Alzheimer's disease and synapse Loss: What can we learn from induced pluripotent stem Cells?

Autores de CIPF

• 

  Francisco Rodríguez Jiménez

  Autor

• 

  Slaven Erceg Vukicevic

  Autor

Participantes ajenos a CIPF

• Ureña-Peralta J
• Jendelova P

Grupos de Investigación

• Laboratorio Terapias con Células Madre en Enfermedades Neurodegenerativas

  

  Jefe/a de Grupo

  Slaven Erceg Vukicevic

Abstract

Synaptic dysfunction is a major contributor to Alzheimers disease (AD) pathogenesis in addition to the formation of neuritic ß-amyloid plaques and neurofibrillary tangles of hyperphosphorylated Tau protein. However, how these features contribute to synaptic dysfunction and axonal loss remains unclear. While years of considerable effort have been devoted to gaining an improved understanding of this devastating disease, the unavailability of patient-derived tissues, considerable genetic heterogeneity, and lack of animal models that faithfully recapitulate human AD have hampered the development of effective treatment options. Ongoing progress in human induced pluripotent stem cell (hiPSC) technology has permitted the derivation of patient- and disease-specific stem cells with unlimited self-renewal capacity. These cells can differentiate into AD-affected cell types, which support studies of disease mechanisms, drug discovery, and the development of cell replacement therapies in traditional and advanced cell culture models.

Keywords

• Alzheimer's disease, Astrocytes, Brain organoids, Induced pluripotent stem cells, Microglia, Neural differentiation, Neuronal loss, Neurons