Frontotemporal dementia, one of the most common causes for early-onset dementia, may be linked to an overactive immune system, a new study found.
For the study, published in the Journal of Neurology, researchers at the University of Eastern Finland recruited 98 patients with frontotemporal dementia, diagnosed between 1998 and 2016.
According to researchers, the primary aim was to examine any possible inflammatory changes in the blood of samples of patients, correlating specific markers to numerous clinical features of frontotemporal dementia, such as motoneuron and Parkinsonism symptoms.
Using the Mini-Mental State Examination (MMSE) and Activities of Daily Living Scale (ADCS), researchers were able to measure the progression of the degenerative disease, investigating cytokine or chemokine levels correlated with cognitive decline.
Moreover, researchers also focused on immune system activity in patients with frontotemporal dementia, examining any comorbidities, including those carrying the C9orf72 repeat expansion.
Based on the findings: “A history of an autoimmune disease was detected in 11 patients, but the measured inflammatory marker levels did not differ in these patients compared to those without autoimmune disease,” wrote Anne Remes, the study’s co-author. “Three patients had systemic immunomodulatory medication but showed no distinct differences in the marker levels compared to the other patients.”
“We then investigated whether the measured cytokine or chemokine levels associated with cognitive or functional decline using MMSE and ADCS-ADL, respectively. None of the cytokines showed correlation with baseline MMSE or ADCS-ADL scores.”
The findings suggest that immune system alterations may be linked to sporadic and genetic types of frontotemporal dementia.
“Our study provides novel information on the associations between inflammation and several carefully defined clinical features and disease progression,” the results detailed.
“Future longitudinal studies in other cohorts are warranted to confirm the suggested correlation of the inflammatory profiles and clinical manifestations in FTLD in general and in FTLD patients carrying the C9orf72 HRE.”
