2012
DOI: 10.1523/jneurosci.0234-12.2012
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Abstract: Parkinson's disease (PD) is the most common representative of a group of disorders known as synucleinopathies, in which misfolding and aggregation of ␣-synuclein (a-syn) in various brain regions is the major pathological hallmark. Indeed, the motor symptoms in PD are caused by a heterogeneous degeneration of brain neurons not only in substantia nigra pars compacta but also in other extrastriatal areas of the brain. In addition to the well known motor dysfunction in PD patients, cognitive deficits and memory im… Show more

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Cited by 231 publications
(196 citation statements)
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“…Studies with PD models indicate that oligomeric α -Syn is the form most likely responsible for neuronal death (Danzer et al, 2007; Winner et al, 2011; Luth et al, 2014). But, studies also indicate that α -Syn monomers are neurotoxic at increased levels (Diógenes et al, 2012; Stoica et al, 2012). As secondary brain damage after transient MCAO occurs at a rapid pace during the first day of reperfusion and at a slower rate between days 1 and 3 of reperfusion, it is likely that both monomers and oligomers of α -Syn play discrete roles in neuronal death after stroke.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Studies with PD models indicate that oligomeric α -Syn is the form most likely responsible for neuronal death (Danzer et al, 2007; Winner et al, 2011; Luth et al, 2014). But, studies also indicate that α -Syn monomers are neurotoxic at increased levels (Diógenes et al, 2012; Stoica et al, 2012). As secondary brain damage after transient MCAO occurs at a rapid pace during the first day of reperfusion and at a slower rate between days 1 and 3 of reperfusion, it is likely that both monomers and oligomers of α -Syn play discrete roles in neuronal death after stroke.…”
Section: Discussionmentioning
confidence: 99%
“…Under native conditions, α -Syn is known to exist as a helically folded tetramer that resists aggregation (Bartels et al, 2011). But inactivation of N and C terminals due to post-translational modifications disrupts stability of the tetrameric structure and leads to oligomerization and aggregation of α -Syn, which are thought to be responsible for its toxicity; however, increased levels of α -Syn monomers also promote neuronal death (Diógenes et al, 2012; Stoica et al, 2012). …”
Section: Introductionmentioning
confidence: 99%
“…However, it has been reported that extracellular and intracellular α-syn can promote clathrin-mediated NMDAR endocytosis and counteract NMDAR-mediated dopaminergic cell death (Cheng et al, 2011). Moreover, extracellular α-syn oligomers can modulate synaptic transmission and impair long term potentiation (LTP) via NMDAR activation (Diogenes et al, 2012). Collectively, these evidences suggest that α-syn and its C-terminally truncated form can regulate NMDARs function, and may thus crucially affect the fate of glutamateinduced responses in neuronal cells.…”
Section: Introductionmentioning
confidence: 99%
“…For example, in next generation designs the trident structures can be replaced with one outgrowth channel per neuron to reduce the probability of multiple axons forming bundles. These capabilities can greatly benefit a variety of neuroscience applications, including; nanoparticulate toxicity 24 and manganese propagation 25 , activity synchronization in epilepsy, the dissemination of infectious agents such as prions 26 , amyloid beta (Ab) transmission in Alzheimer disease 9 , and alpha synuclein in Parkinson disease 27 .…”
Section: Discussionmentioning
confidence: 99%