Lab Mission

Research Goal

Neurodegenerative diseases are currently the most debilitating adult-onset illnesses affecting millions of people worldwide, with an increasing prevalence due to extensions in the lifespan. Among the variety of functional impairments elicited by neurodegeneration, the progressive loss of the ability to communicate has been self-reported by patients as one of the most devastating consequences of neurodegenerative diseases, significantly impacting their psychosocial health, independent functioning, and quality of life. Due to the lack of medical cure, behavioral interventions, including compensatory strategies and exercise-based training, combined with voice banking and augmentative and alternative communication (AAC), currently constitute the mainstay of managing progressive communication disorders in neurodegenerative diseases. The overarching goal of these interventions is to help patients maintain functional communication throughout the disease course, allowing them to preserve independence and retain basic societal roles for a meaningful quality of life for as long as possible. Toward this goal, a central need is for a personalized care approach to deliver the right intervention to the right person at the right time, in order to meet the evolving communication needs of an individual across all stages of disease progression. The implementation of this approach, however, has proven a significant clinical challenge, due to the profound heterogeneity of neurodegenerative diseases, resulting in highly variable profiles of communication disorders that remain hard to understand, delineate, and characterize based on the current clinical standards.

The heterogeneity of neurodegenerative diseases stems from a complex dynamic interplay of pathological, genetic, environmental, biological, and demographic factors. In the spatial domain, various pathological processes (e.g., Tau, TDP-43, alpha-synuclein, beta amyloid) have been associated with neurodegeneration. These pathological processes spread across distributed neural networks related to motor, cognitive, language, affective, and behavioral functions. The resulting neurophysiological changes can differentially affect multiple domains of communicative function (e.g., motor speech, cognitive-linguistic), contributing to heterogeneity in phenotypic characteristics. In the temporal domain, subclinical neurophysiological changes emerge early during the prodromal phase, long before the clinical diagnosis. After a variable period of progression, these subclinical changes eventually culminate in clinical symptoms and functional declines. The differential rate of progression contributes to the temporal heterogeneity of neurodegenerative diseases.

Collectively, the phenotypic and temporal heterogeneities lead to highly variable clinical manifestations and prognostic trajectories of progressive communication disorders, posing a significant challenge to personalized care. To address this challenge, improved diagnostic, prognostic, and phenotyping models of progressive communication disorders are critically needed to capture and document subclinical changes across all domains of communicative function throughout both prodromal and symptomatic phases. Such models will enhance personalized care for progressive communication disorders, by (1) improving screening, early detection, and intervention planning, to maximize the neuroprotective and symptom-ameliorating effects of intervention strategies (before the disease has progressed too far); (2) enhancing patient definition and subtyping, to guide clinicians in tailoring interventions to individual-specific deficits for optimal outcomes.