Eyeblink classical conditioning in Alzheimer's disease and cerebrovascular dementia

Eyeblink classical conditioning (EBCC) is severely and consistently impaired in probable Alzheimer's disease (AD), presumably due to normal age related changes in the cerebellum and AD-related hippocampal cholinergic disruption. Less consistent impairment and more variable EBCC performance was predicted in patients with cerebrovascular dementia (CVD) because some CVD patients should have impairment in EBCC when their lesions affect the EBCC circuitry, whereas others with lesions in noncritical regions should have normal EBCC. As predicted, variability in EBCC performance was greater in patients with CVD than in probable AD patients. Acquisition of conditioned responses in the group of CVD patients was better than in the probable AD group. These data show in another sample of normal control subjects and probable AD patients that EBCC has a high sensitivity for probable AD.

[1]  A. K. Miller,et al.  VARIATIONS IN THE HUMAN PURKINJE CELL POPULATION ACCORDING TO AGE AND SEX , 1975 .

[2]  J. Simpson,et al.  Catecholamines and cholinergic enzymes in pre-senile and senile Alzheimer-type dementia and down's syndrome , 1983, Brain Research.

[3]  JOHN W. Moore,et al.  Central cholinergic blockade by scopolamine and habituation, classical conditioning, and latent inhibition of the rabbit’s nictitating membrane response , 1976 .

[4]  P. Solomon,et al.  Disruption of classical conditioning in patients with Alzheimer's disease , 1991, Neurobiology of Aging.

[5]  D. Woodruff-Pak,et al.  Training to criterion in eyeblink classical conditioning in Alzheimer's disease, Down's syndrome with Alzheimer's disease, and healthy elderly. , 1996, Behavioral neuroscience.

[6]  John Madden,et al.  Neurobiology of learning, emotion, and affect , 1991 .

[7]  E. Warrington,et al.  Conditioning in amnesic patients , 1979, Neuropsychologia.

[8]  Z. Khachaturian Diagnosis of Alzheimer's disease. , 1985, Archives of neurology.

[9]  P. Solomon,et al.  Altered activity in the hippocampus is more detrimental to classical conditioning than removing the structure. , 1983, Science.

[10]  D. Woodruff-Pak,et al.  Alzheimer's disease and eyeblink conditioning: 750 ms trace vs. 400 ms delay paradigm , 1996, Neurobiology of Aging.

[11]  R. F. Thompson,et al.  Neuronal responses of the rabbit cerebellum during acquisition and performance of a classically conditioned nictitating membrane-eyelid response , 1984, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[12]  R. F. Thompson,et al.  Cerebellum: essential involvement in the classically conditioned eyelid response. , 1984, Science.

[13]  D. Woodruff-Pak,et al.  Eyeblink conditioning discriminates Alzheimer's patients from non-demented aged. , 1990, Neuroreport.

[14]  J. Simpson,et al.  ALZHEIMER-LIKE CHOLINERGIC DEFICIENCY IN DOWN SYNDROME , 1980, The Lancet.

[15]  J. Brust Vascular dementia is overdiagnosed. , 1988, Archives of neurology.

[16]  R. F. Thompson,et al.  Mammalian brain substrates of aversive classical conditioning. , 1993, Annual review of psychology.

[17]  B J Anderson,et al.  Cerebellar and Brainstem Circuits Involved in Classical Eyeblink Conditioning , 1994, Reviews in the neurosciences.

[18]  I. Daum,et al.  Classical conditioning in patients with severe memory problems. , 1989, Journal of neurology, neurosurgery, and psychiatry.

[19]  D. Woodruff-Pak,et al.  Purkinje cell number related to rate of classical conditioning. , 1990, Neuroreport.

[20]  H. Wiśniewski,et al.  Occurrence of neuropathological changes and dementia of Alzheimer's disease in Down's syndrome , 1985, Annals of neurology.

[21]  J. Cantor,et al.  Concomitant eyeblink and heart rate classical conditioning in young, middle-aged, and elderly human subjects. , 1993, Psychology and aging.

[22]  Y. Li,et al.  Nicotinic cholinergic system involvement in eyeblink classical conditioning in rabbits. , 1994, Behavioral neuroscience.

[23]  N Birbaumer,et al.  Classical conditioning after cerebellar lesions in humans. , 1993, Behavioral neuroscience.

[24]  Scott T. Grafton,et al.  Functional anatomy of human eyeblink conditioning determined with regional cerebral glucose metabolism and positron-emission tomography. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[25]  A. Burns Clinical diagnosis of Alzheimer's disease , 1991 .

[26]  P. Solomon,et al.  Classical conditioning in patients with Alzheimer's disease: a multiday study. , 1995, Psychology and aging.

[27]  M. Roth,et al.  The Association Between Quantitative Measures of Dementia and of Senile Change in the Cerebral Grey Matter of Elderly Subjects , 1968, British Journal of Psychiatry.

[28]  John Q. Trojanowski,et al.  Amyloid plaques in cerebellar cortex and the integrity of Purkinje cell dendrites , 1994, Neurobiology of Aging.

[29]  R. F. Thompson,et al.  Organization of memory traces in the mammalian brain. , 1994, Annual review of neuroscience.

[30]  D. Woodruff-Pak,et al.  Longitudinal investigation of eyeblink classical conditioning in elderly human subjects. , 1995, The journals of gerontology. Series B, Psychological sciences and social sciences.

[31]  M. Hallett,et al.  Deficit in classical conditioning in patients with cerebellar degeneration. , 1993, Brain : a journal of neurology.

[32]  I. Daum,et al.  Classical conditioning after temporal lobe lesions in man: impairment in conditional discrimination. , 1991, Behavioral neuroscience.

[33]  P. Solomon,et al.  Disruption of human eyeblink conditioning after central cholinergic blockade with scopolamine. , 1993, Behavioral neuroscience.

[34]  J. Simpkins,et al.  Novel Approaches to the Treatment of Alzheimer’s Disease , 2012, Advances in Behavioral Biology.

[35]  J. Theios,et al.  Acquisition and extinction of a classically conditioned response in hippocampectomized rabbits (Oryctolagus cuniculus). , 1972, Journal of comparative and physiological psychology.

[36]  J. Andersson,et al.  Brain substrates of aversive classical conditioning. , 1995 .

[37]  I. Katz,et al.  A Model System Demonstrating Parallels in Animal and Human Aging: Extension to Alzheimer’s Disease , 1989 .

[38]  D. Woodruff-Pak,et al.  Eyeblink classical conditioning in H.M.: delay and trace paradigms. , 1993, Behavioral neuroscience.

[39]  Lynn Nadel,et al.  The Psychobiology of Down syndrome , 1988 .

[40]  M. Folstein,et al.  Clinical diagnosis of Alzheimer's disease , 1984, Neurology.

[41]  R. Ivry,et al.  Selective disruption of eyeblink classical conditioning by concurrent tapping , 1995, Neuroreport.

[42]  I. Gormezano,et al.  Effects of scopolamine and methylscopolamine on classical conditioning of the rabbit nictitating membrane response. , 1983, The Journal of pharmacology and experimental therapeutics.

[43]  B. Schreurs,et al.  A functional anatomical study of associative learning in humans. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[44]  David A. McCormick,et al.  Ipsilateral cerebellar lesions prevent learning of the classically conditioned nictitating membrane/eyelid response , 1982, Brain Research.

[45]  J. Steinmetz,et al.  Acquisition of classical conditioning without cerebellar cortex , 1989, Behavioural Brain Research.

[46]  Richard B. Ivry,et al.  Cerebellar involvement in eyeblink classical conditioning in humans. , 1996 .