Age-related neurodegenerative disease pathogenesis remains a hot topic for scientists as there are many ways to approach it: genome instability, protein misfolding, and neuronal defects, to name a few. There is, however, a consensus that dysfunctional autophagy is ubiquitous in neurodegenerative disease. Autophagy, the degradation of intracellular material, maintains homeostasis amidst cellular stress, yet its efficiency is lowered in diseases like Alzheimer’s and Parkinson’s. As cell stress accumulates over natural aging, how autophagy fails under cell stress overload is a key question for researchers. In neurodegenerative disease, there are multiple cell stressors present, three of which we will address: nutrient stress, endoplasmic reticulum (ER) stress, and mitochondrial stress. This review will examine three major autophagy pathways that respond to these stressors respectively—lipophagy, ER-phagy, and mitophagy—and their relationship with one another. Research typically focuses on individual autophagy mechanisms, but there is a lack of research on how these autophagy pathways relate to one another. We identify the nuclear-ER-vacuole junction as an intersection between lipophagy and ER-phagy, but it is harder to connect mitophagy with the two. While mitophagy also requires core autophagy machinery, it specifically relies on the cortical-ER instead of the nuclear-ER. How these connections are affected by neurodegenerative disease is less explored. As there are many different cell stressors present in neurodegenerative disease, the lack of a unifying approach to explain its pathogenesis emphasizes a need for future research that addresses the effects of simultaneous cell stress pathways on autophagy.