William Heindel

Professor & Chair
William_Heindel@brown.edu
(401) 863-9715
Office Location: 
Metcalf 345
Research Focus: 
Neuropsychology of memory and attention, Alzheimer’s disease

 

William Heindel is a cognitive neuroscientist with research interests in human memory, attention and perception in both neurologically intact individuals and brain-damaged patients with neurocognitive disorders. Dr. Heindel received a B.S. in engineering from the University of Wisconsin-Madison in 1980, and a Ph.D. in neurosciences from the University of California, San Diego in 1989. He came to Brown in 1992 following postdoctoral training in neuroimaging and neuropsychology at UCSD. In addition to his research activities, he is also currently serving as Chair of the Department of Cognitive, Linguistic, and Psychological Sciences.

Research Interests:

My research is currently focused on investigating the differential effects of aging and neurological disease on semantic memory, attention, and sensory integration using a variety of methodological approaches including cognitive neuropsychology, electrophysiology (EEG), and functional brain imaging (fMRI). In addition to studying patient populations as model systems for understanding the neural substrates mediating normal cognitive function, my research is also concerned with the development of novel neurocognitive markers and therapeutic approaches for detecting and treating Alzheimer's disease and other neurological disorders.

Some of my current research projects are:

● Investigations of the Perceptual Basis of Semantic Memory

A view of semantic memory as grounded in perception has emerged, based mainly on recent neuroimaging (i.e., fMRI) evidence that retrieval from semantic memory activates unimodal perceptual cortex. Current studies in my lab are investigating this issue through complementary high-temporal resolution behavioral and electrophysiological measures of online semantic processing. Results from these studies are generally supportive of a distributed perceptual-feature model of semantic memory. 

● Neuropsychological Substrates underlying Category Learning

There are several lines of evidence to suggest that categorical information about objects can be acquired either through an explicit system that mediates the use of conscious strategies to categorize stimuli or through an implicit system that mediates unconscious categorization. However, the defining features of these different systems as well as the conditions under which they may interact and contribute to category learning remain unresolved. Research in my lab addresses this issue by: 1) exploring the conditions under which explicit and implicit category learning systems are recruited in normal populations; and 2) examining patterns of category learning performance in patient populations with specific neurological damage to on or the other system mediating category learning.

● Arousal, Attention and Semantic Processing in Alzheimer's Disease

Alzheimer patients' semantic processing impairments in general, and their semantic priming impairments in particular, may be attributable to several distinct factors, including: a) the presence of an actual disruption of semantic memory due to damage to neocortical association areas; b) the presence of selective attentional deficits due to damage within superior parietal regions; and c) the presence of modulatory deficits due to damage within the noradrenergic and cholinergic ascending projection systems. We are currently looking at these different possibilities using a variety of behavioral and electrophysiological techniques that systematically examine how changes in attentional systems influence semantic memory processes in Alzheimer patients.

● Feature Integration and Attention in Alzheimer's Disease

We are looking at the relationship between object representation and visual attention in Alzheimer patients. Although some recent studies suggest that Alzheimer patients possess specific object-based attentional deficits, the disruption of corticocortical connections within higher-order association areas in these patients may also produce impairments in integrating visual information into coherent object representations. Thus, the apparent deficits on tests of visual attention exhibited by Alzheimer patients may be influenced as much by impairments in object representation as by impairments in attention. Identification of the ways in which object representation and attentional processes interact in Alzheimer's disease should not only provide a better understanding of the cognitive deficits associated with this disease, but should also lead to important information about the neuropsychological substrates mediating normal object perception and attention.

● Interactions between Hippocampal and Striatal Memory Systems in ADHD

Although the neuroanatomical underpinnings of ADHD are beginning to be identified, this emerging anatomical model has yet to be integrated with a model of cognitive dysfunction in ADHD. What is critically needed at this time is the development of a coherent conceptual framework for understanding how dysfunction in specific brain networks translates into disordered information processing and thereby into the impulsive and hyperactive behaviors characteristic of ADHD. A potentially fruitful, and as yet unexplored, approach is to view the neuropsychological manifestations of ADHD in terms of interactions between hipppocampal and striatal memory systems. While previous studies in both humans and animals have been successful in identifying and isolating distinct brain systems underlying different forms of memory, relatively few studies have addressed how these distinct learning mechanisms interact to produce coordinated behavioral adaptation to the environment. For example, information acquired through one memory system may either complement or interfere with information acquired through the other memory system, depending on the particular demands of the learning task. Children with ADHD may provide an ideal population to investigate the nature of interactions between distinct memory systems, since unlike other neurological disorders with specific dysfunction within either the hippocampal (e.g., amnesics) or striatal (e.g., Huntington's or Parkinson's disease) memory system, ADHD may best be characterized as a disruption in the normal balance in the activation and utilization of these two learning mechanisms.