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FAD, mit frühem Beginn aufgrund spezifischer Genmutationen, steht im Gegensatz zu SAD, das einen späten Beginn und eine unklare Ursache aufweist. Die Ca2+-Homöostase- Hypothese von SAD legt nahe, dass eine frühzeitige Ca2+-Dysregulation mit der Fehlfaltung von Proteinen und der Anreicherung von Cholesterin einhergeht. Das endoplasmatische Retikulum (ER) ist entscheidend für die Regulation des intrazellulären Ca2+, die Verarbeitung von Proteinen und die Lipid-Biosynthese. Die Familie der transienten Rezeptorpotenzial-Kanäle (TRPC1-7) umfasst TRPC1, der im Hippocampus stark exprimiert wird. Während TRPC2-7 ausschließlich in der Plasmamembran gefunden werden, befindet sich TRPC1 auch in der ER- Membran.\r\nHypothese: TRPC1 könnte an der Regulation von Ca2+, der Synthese von Proteinen und Cholesterin im ER beteiligt sein.\r\nErgebnisse: Vorläufige Experimente zeigten, dass TRPC1 den Ca2+-Leck aus dem ER signifikant verstärkte, den Cholesterinspiegel in TRPC1-transfizierten HEK293-Zellen erhöhte, den Cholesterinspiegel in den Hippocampi transgener Mäuse im Alter veränderte und die Expression von Transkriptionsfaktoren beeinflusste, die an der Proteinfaltung beteiligt sind.\r\nFazit: Eine weitere Erforschung der Rolle von TRPC1 im ER könnte ihn als potenzielles pharmazeutisches Ziel in der AD-Behandlung etablieren.","en":"Background: Alzheimer’s disease (AD) is an irreversible and fatal form of dementia, divided into sporadic (SAD) and familial AD (FAD). FAD, with early onset due to specific gene mutations, contrasts SAD, with late onset and an unclear cause. The Ca2+ homeostasis hypothesis of SAD suggests early Ca2+ dyshomeostasis links to protein misfolding and cholesterol accumulation. The endoplasmic reticulum (ER) is crucial, managing intracellular Ca2+, protein processing, and lipid biosynthesis. The transient receptor potential canonical family (TRPC1-7) includes TRPC1, highly expressed in the hippocampus. While TRPC2-7 target the plasma membrane, TRPC1 is also found in the ER membrane.\r\nHypothesis: TRPC1 may be involved in Ca2+ handling, protein, and cholesterol synthesis in the ER.\r\nResults: Preliminary experiments showed TRPC1 increased Ca2+ leak from the ER, elevated cholesterol in TRPC1- transfected HEK293 cells, altered cholesterol levels in hippocampi from aged transgenic mice, and affected expression of transcription factors involved in protein folding.\r\nConclusion: Further exploring TRPC1 role in the ER could establish it as a potential pharmaceutical target in AD 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