It has been reported that
(+)-MK 801 IGF-1 is associated with several human neurodegenerative diseases [22], [23] and [24]. In Alzheimer disease rodent models, over-expression of IGF-1 rescues amyloid β (Aβ)-induced cell death [25]. De-regulation of the IGF-1 pathway is observed in both type 1 and type 7 spinocerebellar ataxia (SCA) [26]. IGF-1 signaling is also found to suppress neurodegeneration in type 1 spinocerebellar ataxia and Huntington’s disease [27] and [28]. Some studies have also implicated the protective effects of IGFs in PD. It is shown that IGF-1 protects human and rodent neuronal cultures against dopamine induced neurocytotoxicity [29]. Further, studies using rodent models of Parkinson disease demonstrated that activation of IGF signaling pathways exerted neuroprotective effects on dopaminergic
neurons [23] and [30]. We have shown that IGF-1 rescues α-synuclein cytotoxicity and suppresses α-synuclein aggregation through the activation of PI3K/Akt pathways. These results implicate the therapeutic potential of targeting IGF-1/PI3K/Akt pathways in Parkinson disease treatment.
