Changes of Biogenic Amines and Their Metabolites in Postmortem Brains from Patients with Alzheimer‐Type Dementia

Abstract: Noradrenaline (NA), 3,4‐dihydroxyphenyl‐ethylamine (dopamine, DA), 5‐hydroxytryptamine (serotonin, 5‐HT), homovanillic acid (HVA), and 5‐hydroxy‐indoleacetic acid (5‐HIAA) were measured in 22 regions of postmortem brains from four histologically verified cases with Alzheimer‐type dementia (AID) and nine histologically normal controls. Compared with the controls, concentrations of 5‐HT and 5‐HIAA in the ATD brains were significantly reduced in nine regions (superior frontal gyrus, insula, cingulate gyrus, amygdala, putamen, medial and lateral segments of globus pallidus, substantia nigra, lateral nucleus of thalamus) and in eight regions (amygdala, substantia innominata, caudate, putamen, medial and lateral segments of globus pallidus, medial and lateral nuclei of thalamus), respectively. NA concentrations of the ATD brains were significantly reduced in six regions (cingulate gyrus, substantia innominata, putamen, hypothalamus, medial nucleus of thalamus, raphe area). In contrast, significant reductions of DA and HVA concentrations in the ATD brains were found only in putamen and amygdala, respectively. The 5‐HIAA/5‐HT ratio in the ATD brains decreased significantly in locus coeruleus, while the HYA/DA ratio increased significantly in putamen and medial segment of globus pallidus. These findings suggest that the serotonergic and noradrenergic systems are affected, while the dopaminergic system is relatively unaffected in ATD brains.

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

[2]  E. Perry,et al.  Monoamine metabolism in senile dementia of Alzheimer type , 1983, Journal of the Neurological Sciences.

[3]  Marshal F. Folstein,et al.  Aging of the Brain and Dementia , 1983 .

[4]  D. Neary,et al.  Biochemical Assessment of Serotonergic and Cholinergic Dysfunction and Cerebral Atrophy in Alzheimer's Disease , 1983, Journal of neurochemistry.

[5]  G. K. Wilcock,et al.  Plaques, tangles and dementia A quantitative study , 1982, Journal of the Neurological Sciences.

[6]  E. Kandel,et al.  Molecular biology of learning: modulation of transmitter release. , 1982, Science.

[7]  M N Rossor,et al.  A post-mortem study of the cholinergic and GABA systems in senile dementia. , 1982, Brain : a journal of neurology.

[8]  C. Mondadori Pharmacological modulation of memory: trends and problems , 1981, Acta neurologica Scandinavica. Supplementum.

[9]  G. Blessed,et al.  Cell loss in the locus coeruleus in senile dementia of Alzheimer type , 1981, Journal of the Neurological Sciences.

[10]  L. Vachon,et al.  Involvement of serotonin and catecholamine metabolism in cats trained to perform a delayed response task , 1981, Neuroscience.

[11]  T. Crow,et al.  Reduced dopamine-beta-hydroxylase activity in Alzheimer's disease , 1981, British medical journal.

[12]  P. Yates,et al.  Changes in the Monoamine Containing Neurones of the Human Cns in Senile Dementia , 1980, British Journal of Psychiatry.

[13]  J. Simpson,et al.  DOPAMINE IN ALZHEIMER'S DISEASE AND SENILE DEMENTIA , 1979, The Lancet.

[14]  B. Winblad,et al.  Changes in the Brain Catecholamines in Patients with Dementia of Alzheimer Type , 1979, British Journal of Psychiatry.

[15]  E. Spokes An analysis of factors influencing measurements of dopamine, noradrenaline, glutamate decarboxylase and choline acetylase in human post-mortem brain tissue. , 1979, Brain : a journal of neurology.

[16]  R. S. Sloviter,et al.  Postmortem stability of norepinephrine, dopamine, and serotonin in rat brain 1 , 1977, Journal of neurochemistry.

[17]  G. Blessed,et al.  NECROPSY EVIDENCE OF CENTRAL CHOLINERGIC DEFICITS IN SENILE DEMENTIA , 1977, The Lancet.

[18]  P. Davies,et al.  SELECTIVE LOSS OF CENTRAL CHOLINERGIC NEURONS IN ALZHEIMER'S DISEASE , 1976, The Lancet.

[19]  D M Bowen,et al.  Neurotransmitter-related enzymes and indices of hypoxia in senile dementia and other abiotrophies. , 1976, Brain : a journal of neurology.

[20]  P. Mcgeer,et al.  ENZYMES ASSOCIATED WITH THE METABOLISM OF CATECHOLAMINES, ACETYLCHOLINE AND GABA IN HUMAN CONTROLS AND PATIENTS WITH PARKINSON'S DISEASE AND HUNTINGTON'S CHOREA , 1976, Journal of neurochemistry.

[21]  E. Robins,et al.  A STUDY OF SELECTED CATECHOLAMINE METABOLIZING ENZYMES: A COMPARISON OF DEPRESSIVE SUICIDES AND ALCOHOLIC SUICIDES WITH CONTROLS 1 , 1974, Journal of neurochemistry.

[22]  B E Roos,et al.  DETERMINATION OF 5‐HYDROXYTRYPTAMINE, 5‐HYDROXYINDOLEACETIC ACID AND HOMOVANILLIC ACID IN BRAIN TISSUE FROM AN AUTOPSY MATERIAL , 1974, Acta psychiatrica Scandinavica.

[23]  G. Sedvall,et al.  Post-mortal changes of dopamine and homovanillic acid levels in rat striatum as measured by mass fragmentography. , 1974, Brain research.

[24]  C. Gottfries,et al.  The Investigation of Homovanillic Acid in the Human Brain and its Correlation to Senile Dementia , 1969, British Journal of Psychiatry.

[25]  Å. Bertler Occurrence and Localization of Catechol Amines in the Human Brain , 1961 .

[26]  Oliver H. Lowry,et al.  Protein measurement with the Folin phenol reagent. , 1951, The Journal of biological chemistry.

[27]  K. Brodmann Vergleichende Lokalisationslehre der Großhirnrinde : in ihren Prinzipien dargestellt auf Grund des Zellenbaues , 1985 .

[28]  A. D. Smith,et al.  IBRO handbook series. Methods in the neurosciences , 1983 .

[29]  B. Winblad,et al.  Biogenic amines in human brain in normal aging, senile dementia, and chronic alcoholism. , 1980, Advances in biochemical psychopharmacology.

[30]  J. Dahlberg,et al.  Molecular biology. , 1977, Science.

[31]  D. Robinson Changes in monoamine oxidase and monoamines with human development and aging. , 1975, Federation proceedings.