David Salmon, PhD

David Salmon, PhD

 

 

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The primary goal of our research is to understand the organization of memory and cognition in the brain through the psychological and neurological analysis of disorders of these processes in humans. Our research has focused principally on contrasting and comparing the neuropsychological deficits associated with diverse dementing disorders which arise from degeneration of various cortical (e.g., Alzheimer's disease) and subcortical (e.g., Huntington's disease and Parkinson's disease) brain structures. This cognitive neuropsychological approach has led to (1) the provision of neurobiological evidence for the conceptual distinctions that have been drawn among various forms of memory including episodic, semantic and procedural memory; (2) elucidation of the neurological underpinnings of various forms of procedural learning including verbal and non-verbal priming and the acquisition of motor, perceptual and cognitive skills; (3) systematic analysis of the organization and breakdown of semantic memory in individuals with degenerative disease affecting frontal, temporal and parietal cortices; (4) determination of the relationship between disorders of cognition and memory and neuropathological changes in specific brain regions; and (5) the description of the course and progression of cognitive deficits associated with dementia of the Alzheimer type and other disorders of memory and higher order cognitive processes.

Examples of our recent research include studies that demonstrated that the structure of semantic knowledge deteriorates in a systematic manner throughout the course of Alzheimer's disease, presumably because of the progressive destruction of the association cortices in which this knowledge is thought to be stored. Representations of the semantic networks of mildly and moderately demented patients with Alzheimer's disease were generated using multidimensional scaling techniques and it was found that as dementia severity increased, the patients focused less on abstract attributes in categorizing semantic concepts and exhibited an alteration in the relative strength of association between concepts. This disruption of semantic knowledge in patients with Alzheimer's disease was further demonstrated in a study that showed abnormalities in the N400 component of their evoked response, a component that has been linked to the processing of semantic relations between words in studies with normal individuals.

Our research also recently demonstrated that patients with neuropathologically-verified Lewy body variant (LBV) of Alzheimer's disease (i.e., both Alzheimer's and Parkinson's neuropathology in the brain) and diffuse Lewy body disease (DLBD) (i.e., subcortical and diffusely distributed cortical Lewy bodies in the brain) had general cognitive symptoms that were similar to those of patients with "pure" Alzheimer's disease (AD), but that the former two groups had a higher prevalence of visual hallucinations and delusions than the AD patients, and had relatively greater impairment than the AD patients on neuropsychological tests of visuospatial abilities and executive functions. These findings indicated that these clinical and neuropsychological features may be useful for differentiating LBV and DLBD patients from those with "pure" AD and were incorporated into recently developed diagnostic criteria for dementia with Lewy bodies. To further identify neuropsychological deficits that occur in patients with Lewy bodies, we completed a study that demonstrated that patients with Parkinson's disease are impaired on a divided visual attention task, while another group of patients with a subcortical dementia syndrome, patients with Huntington's disease, were not. The visual attention deficit of patients with Parkinson's disease was further demonstrated using a covert orienting of attention task which showed their inability to benefit from cueing when a relatively long interval is interposed between the cue and the target stimulus. This latter finding suggests that these patients may experience a rapid decay of attentional inhibition.

Chan, A.S., Salmon, D.P., Butters, N. and Johnson, S. (1995). Semantic network abnormality predicts rate of decline in patients with probable Alzheimer's disease. J. Internat. Neuropsychol. Soc. 1: 29

Rohrer, D., Wixted, J.T., Salmon, D.P. and Butters, N. (1995). The time course of retrieval from semantic memory and its implications for Alzheimer's disease. J. Exp. Psychol.: Learn. Mem. Cognit. 21:

Salmon, D.P. and Butters, N. (1995). Neurobiology of skill and habit learning. Curr. Opin. Neurobiol. 5: 184-190.

Salmon, D.P., Galasko, D., Hansen, L.A., Masliah, E., Butters, N., Thal, L.J. and Katzman, R. (1996). Neuropsychological deficits associated with diffuse Lewy body disease. Brain Cognit. 31: 148-165.

Stout, J.C., Jernigan, T.L., Archibald, S.L. and Salmon, D.P. (1996). Association of dementia severity with grey matter and white matter hyperintensities in dementia of the Alzheimer type. Arch. Neuro

Iragui, V., Kutas, M. and Salmon, D.P. (1996). Event-related brain potentials during semantic categorization in normal aging and senile dementia of the Alzheimer type. Electroencephalog. Clin. Neuroph

Heindel, W.C., Cahn, D.A. and Salmon, D.P. (1997). Non-associative lexical priming is impaired in Alzheimer's disease. Neuropsychologia 35: 1365-1372.

Heindel, W.C., Salmon, D.P., Fennema-Notestine, C. and Chan, A.S. (1998). Repetition priming with non-verbal stimuli in patients with dementia of the Alzheimer type. Neuropsychology 12: 43-51.