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Synuclein receptor glia

Changyoun Kim, He-Jin Lee, Eliezer Masliah, Seung-Jae Lee
Synucleinopathies are a collection of neurological diseases that are characterized by deposition of α-synuclein aggregates in neurons and glia. These diseases include Parkinson's disease (PD), dementia with Lewy bodies, and multiple system atrophy. Although it has been increasingly clear that α-synuclein is implicated in the pathogenesis of PD and other synucleinopathies, the precise mechanism underlying the disease process remains to be unraveled. The past studies on how α-synuclein exerts pathogenic actions have focused on its direct, cell-autonomous neurotoxic effects...
June 2016: Experimental Neurobiology
Lisa Fellner, Regina Irschick, Kathrin Schanda, Markus Reindl, Lars Klimaschewski, Werner Poewe, Gregor K Wenning, Nadia Stefanova
Alpha-synucleinopathies (ASP) are neurodegenerative disorders, characterized by accumulation of misfolded α-synuclein, selective neuronal loss, and extensive gliosis. It is accepted that microgliosis and astrogliosis contribute to the disease progression in ASP. Toll-like receptors (TLRs) are expressed on cells of the innate immune system, including glia, and TLR4 dysregulation may play a role in ASP pathogenesis. In this study we aimed to define the involvement of TLR4 in microglial and astroglial activation induced by different forms of α-synuclein (full length soluble, fibrillized, and C-terminally truncated)...
March 2013: Glia
Christelle En Lin Chua, Bor Luen Tang
Neuronal dysfunctions and neurodegeneration are often associated with defects in membrane transport. Synucleinopathies are a diverse group of neurodegenerative disorders that share a common pathological feature--insoluble aggregates composed largely of the protein α-synuclein in certain populations of neurons and glia. The actual physiological function of the brain-enriched α-synuclein is still not particularly clear. What is obvious is that when the protein is present in pathologically high amounts, or in mutant forms with enhanced membrane association and oligomerization, it causes neuronal demise with manifestations of impaired neuronal traffic, heightened oxidative stress, mitochondrial degeneration and defects in lipid metabolism...
June 24, 2011: Brain Research Reviews
J B Eells
Transgenic technology, especially the use of homologous recombination to disrupt specific genes to produce knockout mice, has added considerably to the understanding of dopamine (DA) neuron develop, survival and function. The current review summarizes results from knockout mice with the target disruption of genes involved in the development of DA neurons (engrailed 1 and 2, lmx1b, and Nurr1), in maintaining DA neurotransmission (tyrosine hydroxylase, vesicular monoamine transporter, DA transporter, DA D2 and D3 receptors) and important for DA neuron survival (alpha-synuclein, glia cell line-derived neurotrophic factor and superoxide dismutase)...
May 2003: Current Medicinal Chemistry
Atsushi Sakurai, Koichi Okamoto, Masamitsu Yaguchi, Yukio Fujita, Yuji Mizuno, Yoichi Nakazato, Nicholas K Gonatas
The inferior olivary nucleus (ION) from nine patients with multiple system atrophy was examined with antibodies against alpha-synuclein, ubiquitin, synaptophysin, glial fibrillary acidic protein, the Golgi apparatus (GA)-trans-Golgi network (TGN), and microglia/macrophages. As previously reported, there were neuronal loss, gliosis, and alpha-synuclein-positive cytoplasmic inclusions in neurons and glia. In addition, all neurons with alpha-synuclein-positive cytoplasmic inclusions contained abnormal profiles of the GA and TGN, which were reduced in size and numbers...
June 2002: Acta Neuropathologica
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