By Mark Terry
Researchers from Amen Clinics in Costa Mesa, California, Google, Johns Hopkins University, University of California, Los Angeles and the University of California, San Francisco studied 62,454 brain scans of more than 30,000 people to study brain aging.
The brain scans were SPECT (single photon emission computed tomography) scans. The people who participated ranged in age from 9 months to 105 years of age. SPECT tomography reveals regional cerebral blood flow that is reduced in various disorders.
“Based on one of the largest brain imaging studies ever done, we can now track common disorders and behaviors that prematurely age the brain,” said Daniel Amen, founder of Amen Clinics and lead author of the study, in a statement. “Better treatment of these disorders can slow or even halt the process of brain aging. The cannabis abuse finding was especially important, as our culture is starting to see marijuana as an innocuous substance. This study should give us pause about it.”
The study participants also displayed various psychiatric disorders, including bipolar disorder, schizophrenia and attention deficit hyperactivity disorder (ADHD). The study looked at 128 brain regions and attempted to predict the chronological age of the patient. If the scan prediction suggested the patient was older than their actual chronological age, this was interpreted as accelerated brain aging.
Several brain disorders and behaviors predicted accelerated aging. For example, schizophrenia showed an average of 4 years of premature aging. Cannabis abuse showed 2.8 years accelerated aging. Bipolar disorder showed 1.6 years accelerated aging. ADHD showed 1.4 years accelerated aging, and alcohol abuse showed 0.6 years accelerated aging.
One unexpected finding was that depression did not appear to cause accelerated brain aging—and neither did aging.
The study, “Patterns of Regional Cerebral Blood Flow as a Function of Age Throughout the Lifespan” was published in the Journal of Alzheimer’s Disease.
“This is one of the first population-based imaging studies, and these large studies are essential to answer how to maintain brain structure and function during aging,” said George Perry, chief scientist at the Brain Health Consortium from the University of Texas at San Antonio, in a statement. “The effect of modifiable and non-modifiable factors of brain aging will further guide advice to maintain cognitive function.”
The study comes out at the same time as research from MIT’s Picower Institute for Learning and Memory, which suggests that a decrease in the plasticity of specific neurons may be the fundamental cause of normal age-related cognitive decline.
The MIT study tracked the growth and structure of inhibitory interneurons in mice as they aged. The initial data showed no significant drop in the number of inhibitory brain cells as the mice aged. What did show up, however, was a drop in plasticity markers starting around the age of six months, which is considered about middle-aged in mice. (Mice typically live 24 months. Three months is considered mature, 18 months is a senior citizen.)
Between the ages of three and 18 months, the dendrites, the branches that connect neurons, progressively slowed. The researchers wrote in a statement, “Despite common belief, loss of neurons due to cell death is quite limited during normal aging and unlikely to account for age-related functional impairments. Rather, it seems that structural alterations in neuronal morphology and synaptic connections are features most consistently correlated with brain age and may be considered as the potential physical basis for the age-related decline.”
The researchers were able to reverse the aging using fluoxetine, an antidepressant sold under the brand names Prozac and Sarafem. The problem from a practical point of view is these antidepressants aren’t recommended for use in the elderly because of side effects and would have to be administered starting at a young age. However, the fact that it was reversible in laboratory animals shows promise for future research.
The article was published in the Journal of Neuroscience.