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[P4–023]: HIGH‐DEFINITION TRANSCRANIAL DIRECT CURRENT STIMULATION MODULATES BOLD SIGNAL DURING SPATIAL NAVIGATION IN OLDER CONTROLS AND PATIENTS WITH MCI
Author(s) -
Hampstead Benjamin M.,
Lesnovskaya Alina,
Garcia Sarah,
Ma Sean,
Bhaumik Arijit K.,
Giordani Bruno,
Peltier Scott
Publication year - 2017
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.06.1887
Subject(s) - transcranial direct current stimulation , psychology , functional magnetic resonance imaging , neuroscience , spatial memory , inferior parietal lobule , cognition , audiology , stimulation , working memory , medicine
Background:Apathy is the most common neuropsychiatric symptom in Alzheimer’s disease (AD), occurs early in the disease process, and is associated with poor cognitive and functional outcomes. The neurobiological underpinnings for the expression of apathy in AD are not clearly understood and can be assessed via neuroimaging techniques to reveal key mechanisms and treatment targets. Methods: 1. Apathy was assessed in 87 individuals with mild to moderate AD, using the SANS-AD to measure each of the specific cognitive, functional, and emotional domains of apathy. FDG-PET neuroimaging was used to assess the pattern of hypometabolism associated with each apathy domain. 2. Global and individual domains of apathy were measured in 29 individuals with AD. 2FA neuroimaging was used to measure regional a4b2 nicotinic cholinergic receptor binding and to assess relationships between cholinergic receptor binding and the extent of global and domain-specific apathy. 3. A literature review of neuroimaging studies of apathy in AD was performed. Results: Structural and functional imaging studies using MRI, FDG-PET, or perfusion SPECT typically revealed alterations in anterior cingulate, orbitofrontal cortex, and insula associated with apathy in AD. Other frontal regions, temporal cortex, or subcortical nuclei were implicated in some studies, and there was overlap with regions linked to poor insight. Frontal white matter lesions and loss of integrity of white matter tracts on DTI images were also relevant. Associations in MCI were less clear. Apathy was associated with increased global or regional amyloid ligand binding. Each of the three apathy domains was associated with hypometabolism in a unique set of brain regions in AD. Greater apathy was correlated with lower cholinergic binding in middle cingulate and lateral orbitofrontal cortex. Across the neuroimaging studies, relationships were not attributable to depression. Conclusions: Neuroimaging studies indicate that altered structure, function, or neuroreceptor binding in a frontal-limbic-subcortical neural system are associated with apathy in AD. Specific regional alterations drive distinct aspects of apathy and neurotransmitter levels may influence overall tone. Disease-related alterations across this neural system likely promote dysfunction in directed attention, stimulus salience assessment, emotional processing, affective drive, and reward-related decision-making that emerge as clinical apathy in AD.