Semantic Encoding in Alzheimer's Disease and Multi-Infarct Dementia.

86 Pages·2017·2.96 MB·English

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LSU Historical Dissertations and Theses Graduate School
1988
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Bryan Alan Bernard
Louisiana State University and Agricultural & Mechanical College
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Bernard, Bryan Alan, "Semantic Encoding in Alzheimer's Disease and Multi-Infarct Dementia." (1988). LSU
Historical Dissertations and Theses. 4616.
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Semantic encoding in Alzheimer’s disease and multi-infarct
dementia
Bernard, Bryan Alan, Ph.D.
The Louisiana State University and Agricultural and Mechanic,il Col., 1988
U M I
.100 N. Zeeb Rd
Ann Arbor, MI 48109
SEMANTIC ENCODING IN ALZHEIMER'S DISEASE
AND MJIin-INFARCr DEMENTIA
A Dissertation
Submitted to the Graduate Faculty of the
Louisiana State University and
Arts and Sciences College
in partial fulfillment of the
requirements for the degree of
Doctor of Philosophy
in
The Department of Psychology
by
Bryan Alan Bernard
B.S., University of Houston, 1977
M.A., Louisiana State University, 1980
December, 1988
ACKNOWLEDGEMENTS
Very special thanks to my clinical mentor, Bill Waters, who also
served as my advisor and dissertation committee chair, and to Bob
Wilson, who supervised my work at Rusn-Presbyterian-St. Luke's Medical
Center. I could not have oanpleted this project without their help.
Special thanks are also due to Jack Fax, co-director of the Rush
Alzheimer's Disease Center, for his help in selecting subjects.
I wish to sincerely thank the members of my dissertation committee,
Art Riopelle, Don Williamson, Frank Gresham, and Drew Gouvier, who
supported me in this research endeavor.
Thanks to Dorothy Conner for preparation of this rranuscript.
Thanks also to Dave Gilley for statistical assistance and to Skip
Stebbins for his help in preparing the final manuscript.
I wish also to thank Bonnie Hutchison and the staff of the Rush
Alzheimer's Disease Center for their help and support.
Finally, my deepest appreciation to my wife, Linda, and my family
for their unconditional support and encouragement.
ii
TABLE OF OCMTENTS
Page
Ackncwledgements i i
List of Tables........................................... iv
Abstract................................................. v
Introduction ................... 1
Method................................................... 26
Results................................................... 37
Discussion............................................... 46
References............................................... 55
iii
LIST OF TABLES
Table Page
1 Criteria for the Clinical Diagnosis of Alzheimer’s
Disease and Multi-infarct Dementia................... 28
2 Characteristics of Patients with Alzheimer's
Disease, Multi-infarct Dementia, and
Normal Control Subjects............................... 30
3 Performance of the Three Groups on the
Recognition Task..................................... 38
4 Mean Frequency Est urates for the Category
Estimation Task for the Three Groups.................. 40
5 Correlations Between Difference Scores and
Measures of Semantic and Episodic Memory.............. 43
6 Semantic Retrieval Performance for the
Three Groups......................................... 45
iv
ABSTRACT
Episodic and semantic memory tasks were administered to patients
with Alzheimer's disease (AD) and patients with nulti-infarct dementia
(MID) . The MID group had multi-focal lesions predominantly in the
subcortical regions. Episodic memory is recall of events in a
particular temporal-spatial context, whereas semantic memory is
"knewledge" memory regarding words and their associations. The AD and
MID qrtxipe were acmparable in terms of level of deanentia. A control
group of healthy elderly subjects was comparable to the dementia groups
in regard to age and years of education. The experimental measure of
semantic encoding involved presentation of six 14-word lists composed
of exemplarsd rawn from specific semantic categories (e.g.,
vegetables). Following each list, the subjects were required (1) to
rate on a six-point scale the number of exemplars presented for each
category, and then (2) to perform a two-alternative, forced-choice
recognition (episodic memory) task. Although the MID patients were
inpaired on the recognition task, this deficit was not as profound as
that seen in the AD patients. Contrary to predictions, the AD patients
were not markedly insensitive to categorical frequency as compared to
the MID patients, and the measure of semantic processing was correlated
with episodic memory in the normal control amid MID groups but not in
the AD group. The results suggest that poor semantic encoding is
insufficient to explain the episodic memory deficits in AD.
v
As life span continues to increase in modem society, the higher
prevalence and incidence of dementia is being recognized as a major
health problem. Cunmings, Benson, and LoVerme (1980) define dementia
as an acquired persistent inpairment of intellectual function with
ccrpromise in at least three of the following spheres of mental
activity: language, memory, visuospatial skills, emotion or
personality, and cognition (abstraction, calculation, judgment, etc.).
It is estimated that an average of 4.6 percent of persons over age 65
have severe dementia, while just over 10 percent have mild to moderate
dementia (Katzman, 1976; Mortimer, Schuman, & French, 1981). Dementia
is a markedly age-dependent disorder. Although reliable estimates of
the prevalence of dementia among persons under age 65 are difficult to
obtain, this condition is relatively infrequent in the younger
population (Mortimer, 1983) . Each year approximately 1 percent of
those over the age 65 develop dementia, and there is a marked increase
in prevalence between age 70 and 85. By age 80, the probability of a
person developing severe dementia is 15 to 20 percent (Mortimer et al.,
1981). Hie most cannon cause of dementia is Alzheimer's disease (AD),
which accounts for 50 to 60 percent of dementia cases (Katzman, 1986).
Vascular disease, including multi-infarct dementia (MID) and lacunar
states, is the second most cannon cause of dementia, accounting for 10
to 20 percent of the cases.
Alzheimer's disease: Pathological and clinical aspects
The neuropathological hallmarks of AD are neurofibrillary tangles
and neuritic plaques. Neurofibrillary tangles are abnormal nerve cells
in which the cytoplasm is filled with bundles of sutmicrosocpic
1
2
filamentous structures that are wound around each other in a helical
fashion (Wisniewski, Narang, & Terry, 1976) . A neuritic plaque is
corposed of a cluster of degenerating nerve terminals, both dendritic
and axonal, surrounding a core of amyloid protein (Wisniewski & Iqbal,
1980) . Although these changes occur in the aging brain unaccompanied
by dementia, they are more abundant in the brains of demented patients
(Tomlinson, 1977). Neuritic plaques are particularly dense in the
neocortex of demented patients, while the tangles have a predilection
for the hippocanpus. Tangles in the neocortex occur almost exclusively
in demented patients, and are not found in the neooortex of normal
elderly (Terry & Katzman, 1983) . The density of plaques in the cortex
of AD patients at autopsy is highly correlated with the severity of
dementia during life (Blessed, Tomlinson, & Roth, 1968). Biopsy
measures of plaque density have also been reported to correlate highly
with cognitive deficits (Martir. et al., 1987). Other pathological
changes in AD include the presence of amyloid (a waxy, starchlike
substanoe) in seme cerebral and meningeal blood vessels, and
granulcrvacuolar bodies which are found within the cytoplasm of
hippocampal pyramidal cells (Katzman, 1986).
The plaques and tangles are not uniformly distributed throughout
the brain in AD, tending to occur more frequently in cortical
association areas, particularly in the parietal-temporal region (Brun,
1983; Rearson, Esiri, Hioms, Wiloock, & Rowell, 1985; Terry & Katzman,
1983). Primary sensory and motor areas are relatively spared. These
postmortan findings of greater involvement of association areas is
supported by studies using positron emission tomography. For exairple,