The autophagy lysosomal pathway (ALP) is a major mechanism for degrading intracellular macromolecules. The catabolic products can then be used by the cell for energy or as building blocks to make other macromolecules. Since its discovery, a variety of cellular pathways have emerged that target components with varying specificity for lysosomal degradation. Under some circumstances, lysosomes may release their contents into the extracellular space where they may serve signaling or pathogenic functions. The ALP is active in healthy cells, and the level of activity can be regulated by nutrient-sensing and metabolic signaling pathways. The ALP is the primary pathway by which lipids and damaged organelles are degraded and may be the only pathway capable of degrading aggregated proteins. As such, there has been intense interest in understanding the role of the ALP in the accumulation of aggregated misfolded proteins characteristic of many of the major adult-onset neurodegenerative diseases. This review focuses on recent advances in our understanding of the ALP and its potential relationship to the pathogenesis and treatment of neurodegenerative diseases.

中文翻译：

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自噬溶酶体途径和神经变性。

自噬溶酶体途径（ALP）是降解细胞内大分子的主要机制。然后分解代谢产物可以被细胞用作能量或作为构建块来制造其他大分子。自从它被发现以来，已经出现了多种细胞途径，它们针对溶酶体降解具有不同特异性的成分。在某些情况下，溶酶体可能会将其内容物释放到细胞外空间中，在那里它们可以发挥信号传导或致病功能。ALP 在健康细胞中是活跃的，其活性水平可以通过营养感应和代谢信号通路进行调节。ALP 是脂质和受损细胞器降解的主要途径，可能是唯一能够降解聚集蛋白的途径。像这样，人们对了解 ALP 在聚集错误折叠蛋白的积累中的作用有着浓厚的兴趣，这些错误折叠蛋白是许多主要成人神经退行性疾病的特征。本综述侧重于我们对 ALP 及其与神经退行性疾病发病机制和治疗的潜在关系的理解的最新进展。