When they either prevented deltaFosB activity or experimentally increased calbindin expression in the mice,
calbindin levels were restored and the mice improved their memory.
The scientists found the same changes in deltaFosB and
calbindin levels in the hippocampus of Alzheimer's disease patients and in the temporal lobe of epilepsy patients.
Not exact matches
«In fact, we found that when the
levels of deltaFosB increase, those of other proteins, such as
calbindin, decrease.
And when researchers experimentally increased deltaFosB
levels in normal mice,
calbindin expression was suppressed and the animals» memory deteriorated, demonstrating that deltaFosB and
calbindin are key regulators of memory.
«We found that seizures can increase the
levels of deltaFosB in the hippocampus, which results in a decrease in the
levels of
calbindin, a regulator of memory processes.
Aged mutant amyloid precursor protein mice with established disease showed a near complete restoration in
levels of synaptic and neuronal proteins after exposure to young blood in parabiosis (synaptophysin P =.02;
calbindin P =.02) or following intravenous plasma administration (synaptophysin P <.001;
calbindin P =.14).