Longitudinal Multi-Modality Imaging in Progressive Apraxia of Speech
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|ClinicalTrials.gov Identifier: NCT01818661|
Recruitment Status : Recruiting
First Posted : March 26, 2013
Last Update Posted : September 30, 2019
|Condition or disease||Intervention/treatment||Phase|
|PPA Non-fluent Aphasia Apraxia of Speech Primary Progressive Non-fluent Aphasia Primary Progressive Aphasia||Drug: AV-1451||Phase 4|
Apraxia of Speech (AOS) is a disorder of speech motor planning and/or programming that affects the production of speech, characterized by slow speaking rate, abnormal prosody and distorted sound substitutions, additions, repetitions and prolongations, sometimes accompanied by groping, and trial and error articulatory movements. While AOS is commonly associated with vascular insults, it can be the predominant manifestation of neurodegenerative disease. Apraxia of speech can be the only manifestation of a neurodegenerative disorder. However, AOS very often co-occurs with aphasia, particularly a non-fluent aphasia (NFA) of the Broca's type; a language disorder, typically characterized by agrammatic, telegraphic or truncated spoken language, often accompanied by similar difficulties with written language. Patients with neurodegenerative AOS can have varying degrees of NFA, with the aphasia considered more severe than the AOS in some patients, but with the AOS dominant in others. It is extremely rare to have a patient that presents with NFA that does not also have AOS. Patients with isolated AOS can develop NFA over time, although in some patients the AOS remains isolated for as many as 8-10 years.
Patients with AOS can also develop dysarthria and other non-speech motor symptoms, such as extrapyramidal features, postural instability, extra ocular eye movement abnormalities and limb apraxia. Cognitive impairment can also develop, although is rarely an early feature of the disease. The syndrome is progressive with many patients eventually becoming mute.
Studies have shown that patients with neurodegenerative AOS can be pathologically heterogeneous, with some cases showing deposition of the microtubule associated protein tau, while others have deposition of the TAR DNA binding protein of 43kDa (TDP-43). Typical tau pathologies that are observed include corticobasal degeneration, progressive supranuclear palsy (PSP) and Pick's disease. Clinical features are currently unhelpful in predicting the underlying pathology in these cases, although there is a suggestion that cases with isolated or dominant AOS may be more likely to show tau pathology, particularly PSP.
This project will be the first to assess longitudinal multi-modality neuroimaging in subjects with neurodegenerative AOS. It will allow us to assess all aspects of disease progression in these subjects, including changes on neuroimaging, speech and language, neurological, and neuropsychological assessments, to get a complete picture of dysfunction and progression in these subjects. This project will also be the first to apply DTI and the recently developed technique of resting state fMRI to the study of this disease. These techniques are of great current interest to the field and provide, for the first time, a way of assessing underlying functional and structural connectivity across the brain. Both techniques provide important information about how disease progresses through the brain tissue and have huge potential to be important future biomarkers of many different neurodegenerative diseases.
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||50 participants|
|Intervention Model:||Single Group Assignment|
|Masking:||None (Open Label)|
|Official Title:||Longitudinal Multi-Modality Imaging in Progressive Apraxia of Speech|
|Actual Study Start Date :||July 1, 2018|
|Estimated Primary Completion Date :||June 1, 2023|
|Estimated Study Completion Date :||June 1, 2023|
Experimental: Tau positron emission tomography (PET)
All subjects will receive Tau PET scan on approximately day 1 or day 2 of study to assess Tau burden in the brain.
This is used to assess Tau burden in the brain.
- measurement of longitudinal change in neuroimaging and the correlation between change on serial imaging measures and concurrent change on longitudinal measures of clinical performance in neurodegenerative AOS with or without non-fluent aphasia (NFA) [ Time Frame: approxiamtely 1-2 years after baseline imaging ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01818661
|Contact: Sarah Boland, CCRPemail@example.com|
|United States, Minnesota|
|Rochester, Minnesota, United States, 55905|
|Contact: Sarah Boland, CCRP 507-284-3863 firstname.lastname@example.org|
|Principal Investigator:||Jennifer Whitwell, PhD||Mayo Clinic|