| Autor: |
Arnst N; Department of Biomedical Sciences, University of Padova, 35131 Padua, Italy., Redolfi N; Department of Biomedical Sciences, University of Padova, 35131 Padua, Italy., Lia A; Department of Biomedical Sciences, University of Padova, 35131 Padua, Italy.; Neuroscience Institute, Italian National Research Council (CNR), 35131 Padua, Italy., Bedetta M; Department of Biomedical Sciences, University of Padova, 35131 Padua, Italy., Greotti E; Department of Biomedical Sciences, University of Padova, 35131 Padua, Italy.; Neuroscience Institute, Italian National Research Council (CNR), 35131 Padua, Italy.; Padova Neuroscience Center (PNC), University of Padova, 35131 Padua, Italy., Pizzo P; Department of Biomedical Sciences, University of Padova, 35131 Padua, Italy.; Neuroscience Institute, Italian National Research Council (CNR), 35131 Padua, Italy.; Study Centre for Neurodegeneration (CESNE), University of Padova, 35131 Padua, Italy. |
| Abstrakt: |
Alzheimer's disease (AD) is a hereditary and sporadic neurodegenerative illness defined by the gradual and cumulative loss of neurons in specific brain areas. The processes that cause AD are still under investigation and there are no available therapies to halt it. Current progress puts at the forefront the "calcium (Ca 2+ ) hypothesis" as a key AD pathogenic pathway, impacting neuronal, astrocyte and microglial function. In this review, we focused on mitochondrial Ca 2+ alterations in AD, their causes and bioenergetic consequences in neuronal and glial cells, summarizing the possible mechanisms linking detrimental mitochondrial Ca 2+ signals to neuronal death in different experimental AD models. |
