On the other hand, in comparison to non-transgenic (non-Tg) mice, 5xFAD mice, models for mimicking amyloidopathy in AD, manifest prominent synaptosomal mitochondrial dysfunction, and Parkin and LC3BII recruitment in an age-dependent manner, suggesting that synaptosomal mitochondrial deficits are the primary pathology in the Aβ-rich environment, further confirming the relevance of synaptosomal mitochondrial deficits in the development of AD [13]. The gene discussed is PRKN; the disease is Alzheimer disease.