Extensive neuropathological studies have established a compelling link between abnormalities in structure and function of subcortical monoaminergic (MA-ergic) systems and the pathophysiology of Alzheimer's disease (AD). The main cell populations of these systems including the locus coeruleus, the raphe nuclei, and the tuberomamillary nucleus undergo significant degeneration in AD, thereby depriving the hippocampal and cortical neurons from their critical modulatory influence. These studies have been complemented by genome wide association studies linking polymorphisms in key genes involved in the MA-ergic systems and particular behavioral abnormalities in AD. Importantly, several recent studies have shown that improvement of the MA-ergic systems can both restore cognitive function and reduce AD-related pathology in animal models of neurodegeneration. This review aims to explore the link between abnormalities in the MA-ergic systems and AD symptomatology as well as the therapeutic strategies targeting these systems. Furthermore, we will examine possible mechanisms behind basic vulnerability of MA-ergic neurons in AD.
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Ascending monoaminergic systems alterations in Alzheimer's disease. translating basic science into clinical care.
Neurosci Biobehav Rev
September 2013
Department of Physiology, School of Medicine, National University of San Agustin, Arequipa, Peru.
Extensive neuropathological studies have established a compelling link between abnormalities in structure and function of subcortical monoaminergic (MA-ergic) systems and the pathophysiology of Alzheimer's disease (AD). The main cell populations of these systems including the locus coeruleus, the raphe nuclei, and the tuberomamillary nucleus undergo significant degeneration in AD, thereby depriving the hippocampal and cortical neurons from their critical modulatory influence. These studies have been complemented by genome wide association studies linking polymorphisms in key genes involved in the MA-ergic systems and particular behavioral abnormalities in AD.
View Article and Find Full Text PDF[Synthesis of monoamines by non-monoaminergic neurons: illusion or reality?].
J Soc Biol
May 2010
Institut de Biologie du Développement, Académie Russe des Sciences et Institut de Physiologie Normale, Académie Russe des Sciences Médicales, 26 rue Vavilov, 117808 Moscou, Russie.
In contrast to monoaminergic (MA-ergic) neurons possessing the whole set of the enzymes for MA synthesis from the precursor amino-acid, some, mostly peptidergic, neurons co-express only one of the enzymes of monoamine synthesis. They are widely distributed in the brain, being particularly numerous in ontogenesis and, in adulthood, under certain physiological conditions. Most monoenzymatic neurons possess one of the enzymes for dopamine (DA) synthesis, tyrosine hydroxylase (TH) or aromatic L-amino acid decarboxylase (AADC).
View Article and Find Full Text PDFCrossroads of corticotropin releasing hormone, corticosteroids and monoamines. About a biological interface between stress and depression.
Neurotox Res
January 2002
Department of Psychiatry and Neuropsychology, Academic Hospital Maastricht, and the Brain and Behavior Research Institute, Maastricht University, P.O.Box 5800, 6202 AZ Maastricht, The Netherlands.
Mental disorders are frequently preceded by stressful events or situations. Depression is a typical case in point. This raises the question, is depression - or possibly better: are certain forms of depression - caused by stress? Can stress be a true pathogenic factor? Phrased differently: can stress destabilize neuronal systems in the central nervous system to such an extent that depressive symptoms are generated? This question is discussed with the corticotrophin releasing hormone (CRH) and MA systems and hypothalamic-pituitary-adrenal (HPA) axis as major foci.
View Article and Find Full Text PDFNeuroendocrine disorders in depressions and their significance for the monoamine hypothesis of depression.
Acta Psychiatr Scand
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This article discusses the results of recent neuroendocrinological research in depressions. The abnormalities found in a given category of vital depressive patients--cortisol hypersecretion, decreased growth hormone response to insulin hypoglycaemia and decreased luteinizing hormone secretion in menopause--are believed to be due to deficient noradrenalin-(NA)-ergic activity in the hypothalmus. Thus explained, they support the so-called MA (monoamine) hypothesis, which postulates that a functional NA deficiency in the brain plays a role in the pathogenesis of certain types of vital depression.
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