Most everyone of a certain age has had that moment where a forgotten name or set of misplaced keys prompts the question, “Is this the first sign of Alzheimer’s disease?”
It’s a logical question and one that UC Davis neurology professor John Morrison discussed Saturday at a presentation on the aging brain at the Center for Neuroscience in Davis.
He did so in front of an audience of 100, most of whom were in the demographic where the aging brain is a big concern.
Morrison does not believe there is any conclusive evidence to show that a simple lapse of memory is a precursor to Alzheimer’s disease.
“I don’t think people really understand this issue where, in cognitive aging, you have difficulty navigating the world and problems with your memory,” Morrison said. “People think this is a mild form of Alzheimer’s disease or dementia. It’s not.”
Finding out the answers to such issues is at the heart of Morrison’s research at UC Davis, where he’s the head of the National Primate Research Center. Morrison has been using rhesus monkeys and rats in his research to learn how the brain ages, what causes the loss of cognition in older age and how to best keep the brain healthy.
Key to that health: the synapse.
In the brain synapses act like toll-like chemical interchanges between neurons. Without well-formed and well-running synapses, learning, memorizing and long-range planning take longer or become difficult, especially in older adults. Where degeneration of synapses is severe, completing such functions becomes nearly impossible.
“You really have to keep your synapses healthy to keep cognitively healthy,” Morrison said. Central to that health are activity, a healthy cardiovascular system and personal interaction, Morrison said.
The most severe level is when unhealthy synapses lead to neuron death. “You cannot bring dead neurons back,” Morrison said.
There is a burgeoning amount of research being done on synapses and their effect on the aging brain. Researchers are looking into whether there is a link between synapse health and inherited developmental brain disorders and into why structural changes in synapses leave neurons vulnerable to death.
“When you forget where you parked your car, this happens when there is a decrease in the efficiency and plasticity of the synapses,” Morrison said. “But that does not mean you have the neuron death associated with Alzheimer’s,” Morrison said.
With Alzheimer’s disease, extensive neuron death takes place in specific areas of the human brain. “It’s not random,” Morrison said.
More research needs to be done in the area of age-related cognitive decline. It is not well established why or how any age-related cognitive decline can or cannot transition to Alzheimer’s disease, he said.
“One of the problems is we’ve not had many good animal models,” Morrison said.
He believes researchers are getting closer to answers. “We may be on the verge of developing a model with the monkey that allows you to look at that transition, but we’re not there yet,” Morrison said.
Using nonhuman primates is a main research area for Morrison. That research has shown that estrogen therapy can forestall declines in the synapses of post-menopausal women.
To establish that, Morrison did research on 24 rhesus macaque monkeys at the National Primate Center. His findings suggest that post-menopausal monkeys that have been given estrogen on a cyclical basis show less cognitive decline than those that were not given estrogen therapy. Those that were not given the therapy that were older showed a 30 percent decline in cognitive function, he said.