@inbook{afd6a901a11d4a85a6fa3a348f80c17f,
title = "Autonomic Nervous System Dysfunctions as a Basis for a Predictive Model of Risk of Neurological Disorders in Subjects with Prior History of Traumatic Brain Injury: Implications in Alzheimer's Disease",
abstract = "Autonomic dysfunction is very common in patients with dementia, and its presence might also help in differential diagnosis among dementia subtypes. Various central nervous system structures affected in Alzheimer's disease (AD) are also implicated in the central autonomic nervous system (ANS) regulation. For example, deficits in central cholinergic function in AD could likely lead to autonomic dysfunction. We recently developed a simple, readily applicable evaluation for monitoring ANS disturbances in response to traumatic brain injury (TBI). This ability to monitor TBI allows for the possible detection and targeted prevention of long-term, detrimental brain responses caused by TBI that lead to neurodegenerative diseases such as AD. We randomly selected and extracted de-identified medical record information from subjects who have been assessed using the ANS evaluation protocol. Using machine learning strategies in the analysis of information from individual as well as a combination of ANS evaluation protocol components, we identified a novel prediction model that is effective in correctly segregating between cases with or without a documented history of TBI exposure. Results from our study support the hypothesis that trauma-induced ANS dysfunctions may contribute to clinical TBI features. Because autonomic dysfunction is very common in AD patients it is possible that TBI may also contribute to AD and/or other forms of dementia through these novel mechanisms. This study provides a novel prediction model to physiologically assess the likelihood of subjects with prior history of TBI to develop clinical TBI complications, such as AD.",
keywords = "Alzheimer's disease, autonomic nervous system, biomarker, neurodegenerative disorders, risk factor, traumatic brain injury",
author = "Lap Ho and Marc Legere and Tongbin Li and Samara Levine and Ke Hao and Breanna Valcarcel and Pasinetti, {Giulio M.}",
note = "Funding Information: This study was supported by discretionary funding from the Icahn School of Medicine at Mount Sinai to Dr. Giulio Maria Pasinetti and by the Geriatric Research Education and Clinical Centers (GRECC) of the James J. Peters Veterans Affairs Medical Center. In addition, Dr. Pasinetti holds a Career Scientist Award in the Research and Development unit and is the Director of the Basic and Biomedical Research and Training Program, GRECC, James J. Peters Veterans Affairs Medical Center. We acknowledge that the contents of this manuscript do not represent the views of the U.S. Department of Veterans Affairs or the United States Government. The current study was supported, in part, by the Altschul Foundation and VA Grant 1I01BX000870-01A2 to Dr. Giulio Maria Pasinetti. Dr. Ke Hao is partially supported by the National Natural Science Foundation of China (Grant No. 21477087) and by the Ministry of Science and Technology of the People{\textquoteright}s Republic of China (Grant No. 2016YFC0206507). Publisher Copyright: {\textcopyright} 2020 The authors and IOS Press. All rights reserved.",
year = "2020",
doi = "10.3233/AIAD200018",
language = "English",
series = "Advances in Alzheimer's Disease",
publisher = "IOS Press",
pages = "237--247",
editor = "Castellani, {Rudy J.}",
booktitle = "Handbook of Traumatic Brain Injury and Neurodegeneration",
address = "United States",
}