Laboratory-based methods derived from basic emotion research can provide a fine-grained, in vivoassessment of emotional functioning in frontotemporal lobar degeneration (FTLD) and Alzheimer's disease(AD) two of the most common dementing disorders. In the next project period, we will continue and expandthis translational research strategy, using these methods to examine multiple emotion processes (reactivity,regulation, knowledge, socioemotional behavior), multiple emotion response systems (peripheral physiology,expressive behavior, subjective experience, eye movements, language), multiple emotion families (positive,negative, self-conscious emotions), and multiple emotion contexts (intrapersonal and interpersonal) in FTLDpatients, AD patients, and age-matched normal controls. As with the other projects in this renewal, we willincrease our emphasis on: (a) distinguishing between FTLD subtypes of frontotemporal dementia (FTD),progressive non-fluent aphasia (PNFA), and semantic dementia (SD); (b) mapping emotional functioning onto volume loss and hypoperfusion in designated brain regions, and (c) exploring emotional functioning inpatients with amyotrophic lateral sclerosis (ALS). The research addresses six specific aims: (1) to usemethods derived from basic emotion research to evaluate emotional functioning (reactivity, regulation,knowledge) in FTLD and AD; (2) to evaluate social behavior in FTLD and AD patients by studying dyadicinteraction with caregivers; (3) to evaluate relationships between specific regions of brain volume loss andhypoperfusion and attendant deficits in and preservation of emotional functioning and social behavior; (4) todelineate differences in emotional functioning among FTLD subtypes (FTD, PNFA, SD) and between thesesubtypes and ALS; (5) to evaluate the integrity of low-level emotional processes (startle eye-blink modulationby emotion, eye-movement capture by and search patterns for emotional stimuli, preattentive processing ofemotional information) in FTLD and AD; and (6) to determine the relations between neuropsychological andbedside measures of cognitive functioning and laboratory-based assessment of emotional functioning. Thisresearch has significant public health benefits. We believe the findings will prove to be extremely useful inimproving the accuracy of clinical diagnosis, monitoring the course of disease progression, understandingthe basis of symptomatology, evaluating the effectiveness of present and future treatments, and in helpingimprove quality of life for patients and their families.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Research Program Projects (P01)
Project #
2P01AG019724-06
Application #
7264457
Study Section
Special Emphasis Panel (ZAG1-ZIJ-3 (J2))
Project Start
2007-09-01
Project End
2012-08-31
Budget Start
2007-09-01
Budget End
2008-08-31
Support Year
6
Fiscal Year
2007
Total Cost
$174,869
Indirect Cost
Name
University of California San Francisco
Department
Type
DUNS #
094878337
City
San Francisco
State
CA
Country
United States
Zip Code
94143
Geier, Ethan G; Bourdenx, Mathieu; Storm, Nadia J et al. (2018) Rare variants in the neuronal ceroid lipofuscinosis gene MFSD8 are candidate risk factors for frontotemporal dementia. Acta Neuropathol :
Sturm, Virginia E; Brown, Jesse A; Hua, Alice Y et al. (2018) Network Architecture Underlying Basal Autonomic Outflow: Evidence from Frontotemporal Dementia. J Neurosci 38:8943-8955
Karch, Celeste M; Wen, Natalie; Fan, Chun C et al. (2018) Selective Genetic Overlap Between Amyotrophic Lateral Sclerosis and Diseases of the Frontotemporal Dementia Spectrum. JAMA Neurol 75:860-875
Staffaroni, Adam M; Brown, Jesse A; Casaletto, Kaitlin B et al. (2018) The Longitudinal Trajectory of Default Mode Network Connectivity in Healthy Older Adults Varies As a Function of Age and Is Associated with Changes in Episodic Memory and Processing Speed. J Neurosci 38:2809-2817
Seo, Sang Won; Thibodeau, Marie-Pierre; Perry, David C et al. (2018) Early vs late age at onset frontotemporal dementia and frontotemporal lobar degeneration. Neurology 90:e1047-e1056
Santos-Santos, Miguel A; Rabinovici, Gil D; Iaccarino, Leonardo et al. (2018) Rates of Amyloid Imaging Positivity in Patients With Primary Progressive Aphasia. JAMA Neurol 75:342-352
Bergeron, David; Gorno-Tempini, Maria L; Rabinovici, Gil D et al. (2018) Prevalence of amyloid-? pathology in distinct variants of primary progressive aphasia. Ann Neurol 84:729-740
Pottier, Cyril; Zhou, Xiaolai; Perkerson 3rd, Ralph B et al. (2018) Potential genetic modifiers of disease risk and age at onset in patients with frontotemporal lobar degeneration and GRN mutations: a genome-wide association study. Lancet Neurol 17:548-558
Björkhem, Ingemar; Patra, Kalicharan; Boxer, Adam L et al. (2018) 24S-Hydroxycholesterol Correlates With Tau and Is Increased in Cerebrospinal Fluid in Parkinson's Disease and Corticobasal Syndrome. Front Neurol 9:756
Eser, Rana A; Ehrenberg, Alexander J; Petersen, Cathrine et al. (2018) Selective Vulnerability of Brainstem Nuclei in Distinct Tauopathies: A Postmortem Study. J Neuropathol Exp Neurol 77:149-161

Showing the most recent 10 out of 607 publications