0000000000323064
AUTHOR
Sergey Stvolinsky
Chemical intervention in senescence-accelerated mice metabolism for modeling neurodegenerative diseases: an overview
Abstract SAMP1 is a line of inbred mice with a pronounced misbalance between generation and neutralization of reactive oxygen species (ROS) in brain and other tissues. This results in accumulation of molecular defects in lipids, proteins and DNA moieties. The metabolic disorders appear at a very early stage of ontogenic development and induce morphological and behavioral defects manifesting from the fourth month after birth. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment of these mice induced specific changes that closely resembled parkinsonian syndrome. Neuropeptide carnosine prevented toxic effects of MPTP and protected the animals against experimental parkinsonism.
Low in vivo brain glucose consumption and high oxidative stress in accelerated aging
AbstractThe validity of the free radical theory of aging has been recently questioned. Our aim was to test whether there is oxidative stress in tissues critically involved in accelerated aging (senescence-accelerated mice, SAM) and whether this correlates with lower glucose consumption in vivo and behavioural tests. Positron emission tomography shows that brains of old SAM-prone animals consume less glucose than young ones. Behavioural characteristics, mitochondrial peroxide production, and damage in both the central nervous system and bone marrow stem cells also indicate that SAM-prone animals age faster than SAM-resistant ones. Our results support the role of the free radical theory of ag…