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Eur J Pharmacol ; 626(1): 72-82, 2010 Jan 10.
Artigo em Inglês | MEDLINE | ID: mdl-19837053

RESUMO

Major depression (MD) is a severe mental disorder characterized by alterations in mood and cognition, with disease severity correlating inversely with cognition scores. Neuropathology can be found abundantly in the limbic system, which is thought to regulate affect, attention and memory. Hypothalamic-pituitary-adrenal (HPA) axis overdrive, as well as decreased serotonin levels, have often been implicated in the pathogenesis of this illness. Interestingly, there is substantial interaction between these two systems, with receptors of one system influencing the function of the other. This results in impaired neural networks, which give rise to the wide range of depressive symptoms. Recently, it has been implied that MD could serve as a risk factor for developing Alzheimer's disease (AD), with patients suffering from lifetime depression having a twofold higher chance of developing AD and exhibiting more AD-related neuropathology. Modifications in the HPA-axis and the serotonergic system may contribute to the development of cognitive decline and eventually AD. These two systems may therefore be involved in the pathogenesis of both illnesses and could provide a link between MD and AD. Obtaining more knowledge on their interactive role in the relation between MD and AD may eventually aid in the development of more effective treatment strategies.


Assuntos
Doença de Alzheimer , Transtornos Cognitivos , Transtorno Depressivo Maior , Doença de Alzheimer/complicações , Doença de Alzheimer/metabolismo , Doença de Alzheimer/patologia , Doença de Alzheimer/fisiopatologia , Animais , Transtornos Cognitivos/complicações , Transtornos Cognitivos/metabolismo , Transtornos Cognitivos/patologia , Transtornos Cognitivos/fisiopatologia , Transtorno Depressivo Maior/complicações , Transtorno Depressivo Maior/metabolismo , Transtorno Depressivo Maior/patologia , Transtorno Depressivo Maior/fisiopatologia , Glândulas Endócrinas/metabolismo , Glândulas Endócrinas/fisiopatologia , Humanos , Hipotálamo/metabolismo , Hipotálamo/fisiopatologia , Neurotransmissores/metabolismo
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