A feature of the brain’s neurons called dendritic spines may protect against dementia, according to new findings.
Neurofibrillary tangles and amyloid plaques appear in the brains of people with Alzheimer’s, but not everyone who has these formations goes on to develop the disease. Between 30 and 50 percent of patients with the plaques and tangles do not develop Alzheimer’s disease. Why not? Scientists have been looking for the reasons.
Researchers at the University of Alabama at Birmingham found the answer may lie in dendritic spines. The dendritic spines of a neuron help it make connections with other neurons and send information. These parts of the neuron may protect against Alzheimer’s disease.
Dendrites, the branched projections of a neuron that transfer electrochemical stimulation from other neural cells to the cell body, have small membranous protrustions called dendritic spines. Each dendritic spine receives input from a single axon at the synapse. The loss of dendritic spines results in the loss of synapses, which can impair cognition. Logically, subects with normal brains would have healthy dendritic spines, and those with dementia would not. The researchers tested the structures and published the results in the journal Annals of Neurology.
The scientists compared dendritic spines in 21 patients with Alzheimer’s, 8 patients who had Alzheimer’s brain changes but no symptoms, and 12 healthy patients. Using bright-field microscopy, Professor Jeremy Herskowitz and the team took images of the dendritic spines, then used the images to create a 3-D digital reconstruction.
The healthy control subjects had more dendritic spines than the subjects with Alzheimer’s. The subjects with Alzheimer’s brain changes but no symptoms also had more spines than the Alzheimer’s subjects — and almost the same dendritic spine density as the healthy subjects. The group with pathology but no symptoms group had very long dendritic spines, longer than both the other groups.
Longer dendritic spines might indicate greater neuroplasticity — the capacity to change and form new neural connections. Increased neuroplasticity could enable the neurons to bypass plaques and tangles, and still communicate with other neurons. If so, this phenomenon could explain why some people who have Alzheimer’s pathology do not show cognitive impairment.
The research suggests that it may be possible for the brain to rebuild neurons. The information gained in the study may help scientists to develop new therapies, especially when brain changes are detected before symptoms appear.
In 2014, a study at NYU Langone Medical Center in New York, published in the journal Science, showed that getting sleep after learning helps neurons form connections, through dendritic branches, that may help brain cells pass information to each other and facilitate long-term memory.
The scientists observed mice that were genetically modified so a particular protein in their brain cells would fluoresce when viewed with a laser scanning microscope. The fluorescence allowed the team to track the growth of new spines along each branch of a dendrite. The mice sprouted new dendritic spines within 6 hours of learning a new task. Different structural changes occurred for different types of learning.
Healthier and more numerous dendritic spines may be a genetic trait, but the brain also may respond to healthy diet and lifestyle. According to Medical News Today, research suggests that as many as a third of dementia cases can be prevented by regular exercise and an active social life.
For more information on Alzheimer’s and dementia, and care choices, see the Guide To Long Term Care.