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Age-Induced Alterations in Hippocampal Function and Metabolism
Pavan K. Shetty † ;Francesca Galeffi † ;Dennis A. Turner † ;
Neurosurgery and Neurobiology, Duke University Medical Center, Research and Surgery Services, Durham VA Medical Center, Durham
NC 27710, USA ;
Figure 2. The figure summarizes major changes that have been reported during aging processes involving neurons. Schematic drawing illustrates increased L-type calcium
channel expression, increased Ca 2+ entry, calpain activation, unregulated cdk5 activity and accumulation of oxidative damage including protein oxidation and aggregation
leading to decreased LTP retention, higher levels of somatic mtDNA and nuclear DNA mutations, and eventually cognitive function. NMDAR; N-methyl-D-aspartate receptor,
CaMKII; Ca 2+ calmodulin-dependent protein kinase II, cam; calmodulin, Cdk5; cyclin-dependent kinase, ROS; reactive oxygen species, ATP; Adenosine-5′-triphosphate,
mtDNA; Mitochondrial DNA, LTP; long term potentiation, NAD; Nicotinamide adenine dinucleotide, nNOS – neuronal nitric oxide synthetase, TCA cycle; tricarboxylic acid
null,null,2(3),196-218.
Doi:null
cycle, Arg; arginine, HSD;
hypoxic synaptic depression, PARP; Poly ADP-ribose polymerase, SOD; superoxide dismutase, PTP; permeability transition pore.