The Neural Basis of Impaired Affective Prosody in Alzheimer's Disease and Frontotemporal Degeneration

Johns Hopkins University, Baltimore MD

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Abstract

PROJECT SUMMARY Many patients with Alzheimer?s Disease (AD) and Frontotemporal Degeneration (FTD) have impairments in social function, including impaired recognition and expression of emotions in speech. Diminished affective prosody (understanding and conveying emotion through vocal intonation, rate, pauses, and stress) often appears even in the early stages of disease. It is also a common impairment in patients with right hemisphere (RH) strokes. In the parent grant of this supplement, we seek to identify the perceptual, cognitive, and motor deficits that can disrupt affective prosody, and characterize the natural history of spontaneous recovery following a RH stroke. In this Administrative Supplement we extend our research to focus on affective prosody deficits in patients with AD and FTD. Affective prosody deficits can negatively impact social relationships and quality of life in patients with neurodegenerative diseases, and they often lead to more behavioral problems and increased conflict with caregivers. The main objective of this supplement is to identify the perceptual, cognitive, and motor deficits that disrupt affective prosody in AD and FTD, and to identify the neural networks that support these functions. Furthermore, evidence suggests patterns of deficits in expressive and receptive affective prosody differ between the different variants of AD and FTD. Therefore, we will compare patterns of deficits in the following five subtypes of AD and FTD. Two subtypes of AD: (1) typical AD, and (2) logopenic variant Primary Progressive Aphasia (lvPPA); three subtypes of FTD: (1) behavioral variant FTD (bvFTD), (2) nonfluent variant PPA (nfvPPA), and (3) semantic variant PPA (svPPA). PPA is a neurodegenerative syndrome where language impairments are the most prominent deficit in early stages of the disease. In Specific Aim 1 we will identify acoustic abnormalities and the deficit underlying these abnormalities in perception and expression of affective prosody that can be independently damaged by focal atrophy in each subtype. We will also examine the impact of these deficits on quality of life. Patients will be tested on a battery of cognitive and affective prosody tests, developed as part of the parent grant, to identify behavioral patterns of deficits. In Specific Aim 2 we will identify the neural streams necessary for the processes that subserve affective prosody. We will use structural MRI measures to investigate relationships between atrophy patterns and performance on the cognitive and affective prosody tasks. These data will provide robust preliminary data for the submission of a larger grant that will be designed to longitudinally follow patients to identify variation in the course of the disease, and will allow us to better predict to which variant early stage unclassifiable AD and FTD patients will evolve. Our research will also provide the basis for designing future behavioral and neuromodulatory treatments to slow the rate of decline in affective prosody.