Alpha-synuclein (α-Syn) is a major component of Lewy bodies, abnormal protein aggregates that are present in neurons of patients with Parkinson’s disease and other neurological disorders. Despite intensive investigation, the in vivo role of α-Syn in physiological and pathological processes is not fully understood. This study addresses a current debate on the nuclear localization of α-Syn protein in the brain. To assess the specificity of various α-Syn antibodies, we compared their staining patterns in wild type mouse brains with that of the α-Syn knock-out mice. Among five different α-Syn antibodies tested here, two generated intensive nuclear staining throughout the normal mouse brain. However, nuclear staining by these two antibodies was also present in neurons of the α-Syn knock-out mice. This provides evidence that the nuclear signal is not specifically related to the presence of α-Syn, but rather results from the cross-reactivity of the two antibodies to some unknown antigens in neuronal nuclei. In mouse brain neurons, endogenous α-Syn proteins are primarily localized to neuronal processes and nerve terminals but present only at low levels in the cell bodies. This is different from a generally uniform distribution of exogenously expressed α-Syn in both cytoplasm and nuclei of heterologous cells, and suggests that the neuritic enrichment of α-Syn in neurons may be mediated by their specific interactions with certain structural or molecular components in the neuropil.
Alzheimer's disease is an irreversible, progressive neurodegenerative disorder leading invariably to death, usually within 7-10 years after diagnosis and is the leading cause of dementia in the elderly. Not only is Alzheimer's disease a tragic disease in which people suffer from neurodegeneration in the years to come, it also becomes an incredible burden on the public health system. However, there is currently no effective treatment to halt the progression or prevent the onset of Alzheimer's disease. This is partly due to the fact that the complex pathophysiology of Alzheimer's disease is not yet completely understood. Recently, Golgi apparatus is found to play an important role in Alzheimer's disease. In this review, we discuss the changes of Golgi apparatus during clinical progression and pathological development of Alzheimer's disease. First, changes of Golgi apparatus size in Alzheimer's disease are summarized. We then address the role of Golgi apparatus in the neuropathology of Alzheimer's disease. Finally, the role of Golgi apparatus in the pathogenesis of Alzheimer's disease is discussed. Understanding the contribution of Golgi apparatus dysfunction to Alzheimer's disease and its pathophysiological basis will significantly impact our ability to develop more effective therapies for Alzheimer's disease.
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