Brain activation in frontotemporal and Alzheimer’s dementia: a functional near-infrared spectroscopy study

Abstract Background Frontotemporal dementia is an increasingly studied disease, the underlying functional impairments on a neurobiological level of which have not been fully understood. Patients with the behavioral-subtype frontotemporal dementia (bvFTD) are particularly challenging for clinical measurements such as functional imaging due to their behavioral symptoms. Here, an alternative imaging method, functional near-infrared spectroscopy (fNIRS), is introduced to measure task-related cortical brain activation based on blood oxygenation. The current study investigated differences in cortical activation patterns of patients with bvFTD, Alzheimer’s dementia (AD), and healthy elderly subjects measured by fNIRS. Method Eight probable bvFTD patients completed the semantic, phonological, and control conditions of a verbal fluency task. Eight AD patients and eight healthy controls were compared on the same task. Simultaneously, an fNIRS measurement was conducted and analyzed using a correction method based on the expected negative correlation between oxygenated and deoxygenated hemoglobin. Results Healthy controls show an increase in cortical activation measured in frontoparietal areas such as the dorsolateral prefrontal cortex. The activation pattern of patients with AD is similar, but weaker. In contrast, bvFTD patients show a more frontopolar pattern, with activation of Broca’s area, instead of the dorsolateral prefrontal cortex and the superior temporal gyrus. The frontoparietal compensation mechanisms, seen in the healthy elderly, were missing in bvFTD patients. Conclusion Different frontoparietal cortical activation patterns may indicate a correlate of diverse pathophysiological mechanisms of AD and bvFTD during verbal fluency processing. The AD pattern is weaker and more similar to the healthy pattern, whereas the bvFTD pattern is qualitatively different, namely more frontopolar and without frontoparietal compensation activation. It adheres to a change of cortical activation during the course of the disease.