The normal ageing process is associated with declines in certain cognitive abilities, such as processing speed and certain memory, language, visuospatial, and executive function abilities.
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Scientists have discovered what they believe to be the central mechanism behind cognitive decline associated with normal ageing. The normal ageing process is associated with declines in certain cognitive abilities, such as processing speed and certain memory, language, visuospatial, and executive function abilities.
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Some also experience slowness in thinking and difficulties sustaining attention, multitasking, holding information in mind and word-finding. According to the team from University of Colorado Anschutz Medical Campus, ageing in mice and humans is linked to a specific brain protein including CaMKII.
“The mechanism involves the mis-regulation of a brain protein known as CaMKII which is crucial for memory and learning,” said Ulli Bayer, Professor of pharmacology at the varsity’s School of Medicine. “This study directly suggests specific pharmacological treatment strategies,” Bayer added.
In the study, published in the journal Science Signaling, researchers used mouse models and found that altering the CaMKII brain protein caused similar cognitive effects as those that happen through normal ageing.
Bayer said that ageing in mice and humans both decrease a process known as S-nitrosylation, the modification of a specific brain protein including CaMKII. “The current study now shows a decrease in this modification of CaMKII is sufficient to cause impairments in synaptic plasticity and in memory that are similar in ageing,” Bayer said.
Normal ageing reduces the amount of nitric oxide in the body. That in turn reduces nitrosylation which decreases memory and learning ability, the study said. Bayer said the new research opens the way toward developing drugs and other therapeutic interventions that could normalise the nitrosylation of the protein.
He said that holds out the possibility of treating or staving off normal cognitive decline for an unknown period of time. He pointed out that this would only work in normal age-related cognitive decline, not the decline seen in Alzheimer’s disease and dementia. “We know this protein can be targeted,” Bayer said. “And we think it could be done pharmacologically. That is the next logical step.”
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