Transgenic mice with dysregulated Ca2plus homeostasis in neurons as a model of age-induced neurodegeneration

• Autorzy: Majewski L. , Kuznicki J.
• Języki publikacji: EN

Abstrakty

EN

Altered Ca2+ homeostasis has recently emerged as one of the early events responsible for Alzheimer’s disease (AD). Disturbances in Ca2+ signaling are found before any obvious extracellular Aβ pathology in patients with sporadic AD and it has been shown frequently, that Ca2+ dysfunction augments Aβ formation and Tau hyperphosphorylation. It is suggested, that brain ageing is a result of a subtle, but long-lasting dysregulation of Ca2+ homeostasis in neurons, which may explain that age is the major risk factor in AD. Our group showed that the intracellular Ca2+ level in resting neurons can be modulated by overexpression of STIM proteins. These proteins sense calcium level in ER and are involved in the Store Operated Calcium Entry (SOCE). The objective of our project is to understand how elevated basal Ca2+ level in neurons contributes to neurodegeneration. To achieve this goal constructs for STIM proteins and ORAI1 Ca2+ channels were created and procedures of transgenesis were completed to generate transgenic mice. The animals are now being tested for the transgenes. We will next analyze Ca2+ homeostasis in neurons of the transgenic mice. If they have expected phenotype, other properties will be monitored including behavior and susceptibility to neurodegeneration.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2013
• Tom: 73
• Numer: Suppl.1
• Opis fizyczny: p.55

Twórcy

autor

Majewski L.

• Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology, Warsaw, Poland

autor

Kuznicki J.

• Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology, Warsaw, Poland
• Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland