The role of TLR4 has also been documented in Alzheimer’s disease, where it increases the recognition of fibrillar amyloid-beta (Aβ) [36], while mutations in the NAGLU gene (encoding the enzyme N-acetylglucosaminidase, deficient in MPS type III-B) have been recognized in Parkinson’s disease, suggesting that allelic NAGLU changes may increase patients’ susceptibility to develop Parkinson-like phenotypes due to lysosomal dysfunction [37]. The gene discussed is NAGLU; the disease is Alzheimer disease.