When we talk about dementia today, most of the cases have been identified as Alzheimer’s disease and will occur after age 65 (called late-onset). On April 30th of this year in the issue of Brain (HealthDay News) co-author Dr. Peter Nelson of the University of Kentucky announced a new form of dementia. It affects people above the age of 80, and researchers think it has been around for a long time, probably misdiagnosed as Alzheimer’s disease. Researchers are calling this disease LATE which stands for limbic-predominant age-related TDP-43 encephalopathy.
Instead of amyloid plaques and tau tangles that occur in Alzheimer’s, it is the TDP-43 protein that spreads through the hippocampus and amygdala. These two glands are predominantly involved in memory and learning, so you still have memory loss being exhibited. Dr. Nelson states that approximately 17% of the cases will be due to this protein.
This protein when misfolded is found in amylotropic lateral sclerosis (ALS) and Fronto-temporal lobar disease (FTLD). ALS is known for it’s motor neuron degeneration leading to paralysis, and FTLD is known for symptoms of personality changes and loss of executive function.
Right now the only way to confirm positively the presence of LATE is by autopsy of the brain. Researchers have begun the search for a bio-marker so they can develop a test to identify this new dementia, and to then begin testing various compounds to see if they can halt the protein’s progress.
In hindsight, this could be one reason why drug trials have not been successful in finding a drug that could stop or reverse the damage responsible for dementia. When researchers thought they were dealing with amyloid and tau, they had another protein included in their study that may have very different properties. Instead of this discovery narrowing the field, it has broadened it for us, but at least now studies can be designed to more accurately choose their participants.
LATE is thought to elicit a more gradual decline in memory than Alzheimer’s disease.