Department of Biology, Boston University, 5 Cummington Street, Boston MA 02215, USA.
Trends Mol Med. 2011 Nov;17(11):617-24. doi: 10.1016/j.molmed.2011.06.002. Epub 2011 Jul 26.
The presenilin genes harbor approximately 90% of mutations linked to early-onset familial Alzheimer's disease (FAD), but how these mutations cause the disease is still being debated. Genetic analysis in Drosophila and mice demonstrate that presenilin plays essential roles in synaptic function, learning and memory, as well as neuronal survival in the adult brain, and the FAD-linked mutations alter the normal function of presenilin in these processes. Presenilin has also been reported to regulate the calcium homeostasis of intracellular stores, and presynaptic presenilin controls neurotransmitter release and long-term potentiation through modulation of calcium release from intracellular stores. In this review, we highlight recent advances in deciphering the role of presenilin in synaptic function, calcium regulation and disease, and pose key questions for future studies.
早发性家族性阿尔茨海默病(FAD)相关的基因突变大约 90%发生在早老素基因中,但这些突变如何导致疾病仍存在争议。果蝇和小鼠的遗传学分析表明,早老素在突触功能、学习和记忆以及成年大脑中的神经元存活中发挥着重要作用,而与 FAD 相关的突变改变了早老素在这些过程中的正常功能。早老素还被报道调节细胞内储存的钙稳态,而突触前早老素通过调节细胞内储存的钙释放来控制神经递质释放和长时程增强。在这篇综述中,我们强调了阐明早老素在突触功能、钙调节和疾病中的作用的最新进展,并为未来的研究提出了关键问题。