Alpha Synuclein Oligomers

Our kinetically stable oligomers of alpha-synuclein are generated without an inducer or inhibitor and remain stable for at least 2 weeks at 37oC. They present as globular structures under TEM, demonstrate toxicity in rat primary dopaminergic neurons and induce Parkinson’s-associated alpha synuclein phosphoserine 129 pathology. These oligomers have been previously characterized as globular, cylindrical structures with a beta-sheet structure intermediate between monomers and fibrils, and were demonstrated to have a higher toxicity to neurons than alpha-synuclein fibrils (1,2) . Alpha-Synuclein (SNCA) is expressed predominantly in the brain, where it is concentrated in presynaptic nerve terminals (3) . Alpha-synuclein is highly expressed in the mitochondria of the olfactory bulb, hippocampus, striatum and thalamus (4) . Functionally, it has been shown to significantly interact with tubulin (5), and may serve as a potential microtubule-associated protein. It has also been found to be essential for normal development of the cognitive functions; inactivation may lead to impaired spatial learning and working memory (6) . SNCA fibrillar aggregates represent the major non A-beta component of Alzheimer’s disease amyloid plaque, and a major component of Lewy body inclusions, and Parkinson's disease. Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the progressive accumulation in selected neurons of protein inclusions containing alpha-synuclein and ubiquitin (7, 8) .

Alpha synuclein pre-formed fibrils, Alpha synuclein aggregates, Alpha synuclein protein aggregates, Alpha synuclein aggregates, Alpha-synuclein protein, Non-A beta component of AD amyloid protein, Non-A4 component of amyloid precursor protein, NACP protein, SNCA protein, NACP protein, PARK1 protein, SYN protein, Parkison disease familial 1 Protein

MDVFMKGLSK AKEGVVAAAE KTKQGVAEAA GKTKEGVLYV GSKTKEGVVH GVATVAEKTK EQVTNVGGAV VTGVTAVAQK TVEGAGSIAA ATGFVKKDQL GKNEEGAPQE GILEDMPVDP DNEAYEMPSE EGYQDYEPEA

Neuroscience | Neurodegeneration | Alzheimer's Disease | Tangles & Tau | Neuroscience | Neurodegeneration | Parkinson's Disease | Synuclein | Neuroscience | Neurodegeneration | Multiple System Atrophy

Kinetically stable alpha synuclein oligomers are generated from monomer without an inducer/inhibitor, remain soluble oligomers for at least two weeks at 37 degrees, and are toxic to dopaminergic neurons.

1. Chen, S.W., et. al. (2015). PNAS. E1994-E2003. 2. Lorenzen, N., et. al. (2014). JACS. 136: 3859-3868. 3. “Genetics Home Reference: SNCA”. US National Library of Medicine. (2013). 4. Zhang L., et al. (2008) Brain Res. 1244: 40-52. 5. Alim M.A., et al. (2002) J Biol Chem. 277(3): 2112-2117. 6. Kokhan V.S., Afanasyeva M.A., Van'kin G. (2012) Behav. Brain. Res. 231(1): 226-230. 7. Spillantini M.G., et al. (1997) Nature. 388(6645): 839-840. 8. Mezey E., et al. (1998) Nat Med. 4(7): 755-757.

Kinetically stable alpha synuclein oligomers are generated from monomer without an inducer/inhibitor, remain soluble oligomers for at least two weeks at 37 degrees, and are toxic to dopaminergic neurons.

1. Chen, S.W., et. al. (2015) . PNAS. E1994-E2003. 2. Lorenzen, N., et. al. (2014) . JACS. 136: 3859-3868. 3. “Genetics Home Reference: SNCA”. US National Library of Medicine. (2013) . 4. Zhang L., et al. (2008) Brain Res. 1244: 40-52. 5. Alim M.A., et al. (2002) J Biol Chem. 277 (3) : 2112-2117. 6. Kokhan V.S., Afanasyeva M.A., Van'kin G. (2012) Behav. Brain. Res. 231 (1) : 226-230. 7. Spillantini M.G., et al. (1997) Nature. 388 (6645) : 839-840. 8. Mezey E., et al. (1998) Nat Med. 4 (7) : 755-757.

MDVFMKGLSK AKEGVVAAAE KTKQGVAEAA GKTKEGVLYV GSKTKEGVVH GVATVAEKTK EQVTNVGGAV VTGVTAVAQK TVEGAGSIAA ATGFVKKDQL GKNEEGAPQE GILEDMPVDP DNEAYEMPSE EGYQDYEPEA