Increased p62 levels that indicate autophagosome-lysosome fusion step impairment (and consequent absence of the cargo degradation) have been observed in some neurodegenerative disorders characterized by accumulation of protein aggregates, including Lewy bodies (in Parkinson’s disease), neurofibrillary tangles (in Alzheimer’s disease), Huntingtin aggregates (in Huntington’s disease), and Mallory bodies (in alcoholic and nonalcoholic steatohepatitis) [52,53,54]. This evidence concerns the gene HTT and early-onset autosomal dominant Alzheimer disease.