Academic Journal
Presenilin-2 and Calcium Handling: Molecules, Organelles, Cells and Brain Networks
| العنوان: | Presenilin-2 and Calcium Handling: Molecules, Organelles, Cells and Brain Networks |
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| المؤلفون: | Pizzo P., Basso E., Filadi R., Greotti E., Leparulo A., Pendin D., Redolfi N., Rossini M., Vajente N., Pozzan T., Fasolato C. |
| المساهمون: | Pizzo, P., Basso, E., Filadi, R., Greotti, E., Leparulo, A., Pendin, D., Redolfi, N., Rossini, M., Vajente, N., Pozzan, T., Fasolato, C. |
| بيانات النشر: | NLM (Medline) |
| سنة النشر: | 2020 |
| المجموعة: | Padua Research Archive (IRIS - Università degli Studi di Padova) |
| مصطلحات موضوعية: | Alzheimer’s disease mouse model, autophagy, brain network, calcium signalling, functional connectivity, mitochondria, oscillation, presenilin-2, slow-wave, SOCE |
| الوصف: | Presenilin-2 (PS2) is one of the three proteins that are dominantly mutated in familial Alzheimer's disease (FAD). It forms the catalytic core of the γ-secretase complex-a function shared with its homolog presenilin-1 (PS1)-the enzyme ultimately responsible of amyloid-β (Aβ) formation. Besides its enzymatic activity, PS2 is a multifunctional protein, being specifically involved, independently of γ-secretase activity, in the modulation of several cellular processes, such as Ca2+ signalling, mitochondrial function, inter-organelle communication, and autophagy. As for the former, evidence has accumulated that supports the involvement of PS2 at different levels, ranging from organelle Ca2+ handling to Ca2+ entry through plasma membrane channels. Thus FAD-linked PS2 mutations impact on multiple aspects of cell and tissue physiology, including bioenergetics and brain network excitability. In this contribution, we summarize the main findings on PS2, primarily as a modulator of Ca2+ homeostasis, with particular emphasis on the role of its mutations in the pathogenesis of FAD. Identification of cell pathways and molecules that are specifically targeted by PS2 mutants, as well as of common targets shared with PS1 mutants, will be fundamental to disentangle the complexity of memory loss and brain degeneration that occurs in Alzheimer's disease (AD). |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| Relation: | info:eu-repo/semantics/altIdentifier/pmid/32992716; info:eu-repo/semantics/altIdentifier/wos/WOS:000584022400001; volume:9; issue:10; firstpage:2166; journal:CELLS; http://hdl.handle.net/11577/3358594; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85092502141 |
| DOI: | 10.3390/cells9102166 |
| الاتاحة: | http://hdl.handle.net/11577/3358594 https://doi.org/10.3390/cells9102166 |
| رقم الانضمام: | edsbas.58B7D135 |
| قاعدة البيانات: | BASE |
| DOI: | 10.3390/cells9102166 |
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