Rescue of α-synuclein cytotoxicity by insulin-like growth factors

Kao, Shyan‐Yuan

doi:10.1016/j.bbrc.2009.05.089

Cited by 62 publications

(46 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In vitro models employing oxidative injury or PD mimetics show impressive protection by over-expression of wild-type Akt or by a constitutively active form of Akt (Salinas et al; 2001; Signore et al, 2006; Malagelada et al, 2008; Aleyasin et al, 2010). Similarly, the abilities of a large array of trophic substances and neuroprotective compounds to block death in cellular models of PD are dependent, at least in part, on Akt signaling (Shimoke and Chiba, 2001; Kihara et al, 2002; Hashimoto et al, 2004; Presgraves et al, 2004; Signore et al, 2006; Fernandez-Gomez et al, 2006; Nakaso et al, 2008; Kao, 2009; Tasaki et al, 2010; Malagelada et al, 2010; Steidinger et al, 2011). Collectively, these findings suggest that a common feature of many treatments that are neuroprotective in PD models is their capacity to promote Akt activation.…”

Section: Protective Action Of Enhancing Akt Activity In Pd Modelsmentioning

confidence: 99%

Akt as a Victim, Villain and Potential Hero in Parkinson’s Disease Pathophysiology and Treatment

2011

View full text Add to dashboard Cite

Summary There are two major purposes of this essay. The first is to summarize existing evidence that irrespective of the initiating causes, neuron death and degeneration in Parkinson’s disease (PD) are due to the common feature of failure of signaling by Akt, a kinase involved in neuron survival and maintenance of synaptic contacts. The second is to consider possible means by which such a failure of Akt signaling might be benignly prevented or reversed in neurons affected by PD, so as to treat PD symptoms, block disease progression, and potentially, promote recovery.

show abstract

Section: Protective Action Of Enhancing Akt Activity In Pd Modelsmentioning

confidence: 99%

Akt as a Victim, Villain and Potential Hero in Parkinson’s Disease Pathophysiology and Treatment

2011

View full text Add to dashboard Cite

show abstract

“…1). Pathways of insulin/insulin-like growth factor 1 (Kao, 2009), MAPK (Musgrove et al, 2013), calcium (Melachroinou et al, 2013), apoptosis (Zhou et al, 2006), ubiquitin mediation (Tofaris et al, 2001), dopamine receptor mediation (Wakamatsu et al, 2008), and oxidative stress (Stefanova et al, 2005) had also been proved to play roles in the pathogenesis of α-synucleinopathies. Based on the previous reports, we have the reason to believe the results of our pathway analysis.…”

Section: Discussionmentioning

confidence: 99%

Microarray Expression Analysis for the Paradoxical Roles ofAcanthopanax senticosusHarms in Treating α-Synucleinopathies

Zhang

Lü

et al. 2015

Phytother. Res.

View full text Add to dashboard Cite

α-Synuclein is a key player in the pathogenesis of neurodegenerative disorders with Lewy bodies. Our previous studies have also showed that Acanthopanax senticosus harms (AS) could significantly suppress α-synuclein overexpression and toxicity. Identifying the RNAs related to α-synucleinopathies may facilitate understanding the pathogenesis of the diseases and the safe application of AS in the clinic. Microarray expression profiling of long non-coding RNAs (lncRNAs) and mRNAs was undertaken in control non-transgenic and human α-synuclein transgenic mice. The effects of AS on central nervous system (CNS) in pathology and physiology were investigated based on the lncRNA/mRNA targets analysis. In total, 341 lncRNAs and 279 mRNAs were differentially expressed by α-synuclein stimulus, among which 29 lncRNAs and 25 mRNAs were involved in the anti-α-synucleinopathies mechanism of AS. However, the levels of 19/29 lncRNAs and 12/25 mRNAs in AS group were similar to those in α-synuclein group, which may cause potential neurotoxicity analogous to α-synuclein. This study demonstrated that some of lncRNAs/mRNAs were involved in α-synuclein related pathophysiology, and AS produced the bidirectional effects on CNS under pathological and physiological conditions.

show abstract

“…They noted that IRS-1pS312 staining intensity was higher in glial cytoplasmic inclusion-containing oligodendrocytes compared to oligodendrocytes lacking glial cytoplasmic inclusions in all MSA patients. This is interesting in view of previous in vitro studies showing that reversal of insulin resistance through the activation of the IGF-1 pathway suppresses α-synuclein aggregation and toxicity in neurons (Kao, 2009). It is therefore possible that a similar effect would occur in MSA, where α-synuclein aggregation is a key pathological hallmark.…”

mentioning

confidence: 82%