a(GO:autolysosome)
We found that abundance of autophagic vacuoles (autophagosomes + autolysosomes) significantly increased in cells expressing either of the two tau mutants (Fig. 4d,e). This increase was mainly due to higher content of autolysosomes (red puncta) (Fig. 4d,e), in support of increased macroautophagic flux PubMed:29024336
We found that abundance of autophagic vacuoles (autophagosomes + autolysosomes) significantly increased in cells expressing either of the two tau mutants (Fig. 4d,e). This increase was mainly due to higher content of autolysosomes (red puncta) (Fig. 4d,e), in support of increased macroautophagic flux PubMed:29024336
Pathologically, the AD brains show both accumulated autophagosomes and autolysosomes, suggesting the basal autophagy process in neurons is abnormal in AD (Fig. 3A). PubMed:23528736
Other studies have also demonstrated the accumulation of autolysosomes in the AD brain and experimentally when lysosomal proteolysis is compromised via genetic knockdown of specific cathepsins or use of pharmacological inhibition of lysosomes [2,3,15] PubMed:29758300
Other studies have also demonstrated the accumulation of autolysosomes in the AD brain and experimentally when lysosomal proteolysis is compromised via genetic knockdown of specific cathepsins or use of pharmacological inhibition of lysosomes [2,3,15] PubMed:29758300
In mammals, autophagosomes first fuse with endosomes and multivesicular bodies to form amphisomes, which subsequently fuse with lysosomes to create degradative vacuoles termed autolysosomes [17]. PubMed:18930136
In Huntington’s disease, affected neurons show accumulation of huntingtin in cathepsin-D-positive vacuoles [24]. Cathepsin-D is a lysosomal protease enriched in neuronal tissues, suggesting that these are autolysosomes PubMed:18930136
Other studies have also demonstrated the accumulation of autolysosomes in the AD brain and experimentally when lysosomal proteolysis is compromised via genetic knockdown of specific cathepsins or use of pharmacological inhibition of lysosomes [2,3,15] PubMed:29758300
In Huntington’s disease, affected neurons show accumulation of huntingtin in cathepsin-D-positive vacuoles [24]. Cathepsin-D is a lysosomal protease enriched in neuronal tissues, suggesting that these are autolysosomes PubMed:18930136
CLN3-related neurodegeneration appears to be a consequence of reduced autophagosome-lysosome fusion [42]. PubMed:18930136
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.