Functional improvement in mouse models of familial amyotrophic lateral sclerosis by PEGylated insulin-like growth factor I treatment depends on disease severity.
Stefanie SaengerBettina HoltmannMark R NilgesSusanne SchroederAndreas HoeflichHeidemarie KletzlWill SpoorenSusanne OstrowitzkiTaleen HananiaMichael SendtnerFriedrich MetzgerPublished in: Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases (2012)
Insulin-like growth factor I (IGF-I) has been successfully tested in the SOD1-G93A mouse model of familial amyotrophic lateral sclerosis (ALS) and proposed for clinical treatment. However, beneficial effects required gene therapy or intrathecal application. Circumventing the dosing issues we recently found that polyethylene glycol (PEG) modified IGF-I (PEG-IGF-I) modulated neuromuscular function after systemic application, and protected against disease progression in a motor neuron disease model. Here we investigated its effects in two SOD1-G93A mouse lines, the G1L with a milder and the G1H with a more severe phenotype. Results showed that in G1L mice, PEG-IGF-I treatment significantly improved muscle force, motor coordination and animal survival. In contrast, treatment of G1H mice with PEG-IGF-I or IGF-I even at high doses did not beneficially affect survival or functional outcomes despite increased signalling in brain and spinal cord by both agents. In conclusion, the data point towards further investigation of the therapeutic potential of PEG-IGF-I in ALS patients with less severe clinical phenotypes.
Keyphrases
- amyotrophic lateral sclerosis
- mouse model
- growth hormone
- drug delivery
- spinal cord
- pi k akt
- binding protein
- early onset
- gene therapy
- spinal cord injury
- type diabetes
- skeletal muscle
- machine learning
- multiple sclerosis
- adipose tissue
- cell proliferation
- magnetic resonance
- mass spectrometry
- brain injury
- single molecule
- drug induced
- artificial intelligence
- subarachnoid hemorrhage
- data analysis
- electronic health record
- free survival