At a certain age, the specter of dementia tends to lurk around every obscure corner of our memory banks. It seems these days that I’m often summoning without success a sliver of information or a once-memorable scenario and find myself wondering — even momentarily — whether Alzheimer’s awaits me somewhere down the road.
So, I was encouraged last week by new research out of the Mayo Clinic that may offer physicians a way to disconnect symptoms of memory loss from a dementia diagnosis. The report, published in the journal Brain Communications, identifies a syndrome connected to a particular area of the brain that is more amenable to treatment than Alzheimer’s and offers providers the tools to help them make a more precise diagnosis.
The condition, known as Limbic-predominant Amnestic Neurodegenerative Syndrome (LANS), affects the connection between the brain’s hypothalamus, amygdala, thalamus, and hippocampus. It’s this limbic system that controls everything from hunger and thirst to our urge to procreate. But, because it includes the hippocampus, it also processes memories. And Mayo Clinic neurologist David T. Jones, MD, who led the study, and his crew believe that an accumulation of a protein known as TDP-43 in the limbic system could be the culprit behind LANS.
“In our clinical work, we see patients whose memory symptoms appear to mimic Alzheimer’s disease, but when you look at their brain imaging or biomarkers, it’s clear they don’t have Alzheimer’s.”
“In our clinical work, we see patients whose memory symptoms appear to mimic Alzheimer’s disease, but when you look at their brain imaging or biomarkers, it’s clear they don’t have Alzheimer’s. Until now, there has not been a specific medical diagnosis to point to, but now we can offer them some answers,” Jones explains. “This research creates a precise framework that other medical professionals can use to care for their patients. It has major implications for treatment decisions, including amyloid-lowering drugs and new clinical trials, and counseling on … prognosis, genetics, and other factors.”
Earlier research has shown that Alzheimer’s-related memory loss is typically caused by damage to the neocortical area of the brain rather than to its limbic system. And when Mayo Clinic researchers analyzed the autopsies of more than 200 patients with a history of memory loss but no evidence of Alzheimer’s, they found an abundance of the TDP-43 protein and disproportionate damage to the hippocampus, but few neocortical issues. These patients may have exhibited some mild cognitive impairment, but they did not descend inexorably into deep dementia before their deaths.
Jones admits that more research will be necessary to reinforce the conclusions of this small study, but he envisions a time when clinicians could run a few brain scans and track a few biomarkers to alleviate the concerns of absent-minded seniors like me. “Without a LANS construct, we are left only saying that a patient does not qualify for antiamyloid treatment and that they do not have Alzheimer’s disease,” he writes. “Having a positive diagnosis serves additional utility beyond that and facilitates comprehensive medical care.”
What that care might entail, of course, depends on pinpointing the cause, which could range from medication interactions and infections to mental health issues and traumatic brain injuries. None of those factors come to mind when I consider my own memory lapses, so maybe I’m just growing old. I keep forgetting that.
