Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Int J Geriatr Psychiatry ; 24(11): 1177-84, 2009 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-19274638

RESUMO

BACKGROUND: Apathy has recently been recognized as a distinct clinical syndrome although it is difficult to differentiate from late life depression. In old age, apathy as a syndrome in itself and depression may have different etiologies. Inflammatory markers have been associated with depression in the elderly, but the relation with apathy is unknown. OBJECTIVE: To assess the relation between C-reactive protein (CRP) and apathy as a syndrome in itself, apart from depression, in subjects aged 85 and older. METHODS: All data come from the Leiden 85-Plus Study, a prospective, population-based study of 599 elderly subjects. CRP was measured at baseline. In all subjects with a Mini Mental State Examination (MMSE) > or = 19 points (n = 500), apathy and depression were assessed annually from age 85 to 90 using the three apathy and twelve depression questions of the 15-item Geriatric Depression Scale (GDS-15). The association between CRP and apathy or depressive symptoms was assessed both at baseline and longitudinally. RESULTS: At baseline, no association was found between CRP-concentration and apathy or depression. In subjects free of apathy and depression at baseline, subjects in the highest CRP-tertile at baseline had significantly more increase in depressive symptoms but not in apathy symptoms during follow-up. CONCLUSION: Higher CRP concentrations increased the risk of depression but not apathy in a community-based cohort of 85 years old subjects. This suggests that apathy and depression in old age have different etiologies.


Assuntos
Proteína C-Reativa/metabolismo , Transtorno Depressivo/diagnóstico , Transtornos do Humor/diagnóstico , Idoso de 80 Anos ou mais , Biomarcadores/metabolismo , Transtorno Depressivo/imunologia , Diagnóstico Diferencial , Feminino , Humanos , Imunidade Celular/fisiologia , Masculino , Transtornos do Humor/imunologia , Estudos Prospectivos
2.
Ned Tijdschr Geneeskd ; 152(25): 1413-7, 2008 Jun 21.
Artigo em Holandês | MEDLINE | ID: mdl-18624003

RESUMO

Besides the monoamine hypothesis, the stress hypothesis and the vascular hypothesis, the inflammatory hypothesis might be an etiological explanation for late-life depression. There is a growing amount of evidence to support this hypothesis. In animal studies, injection with cytokines was shown to cause behavioural changes ('sickness behaviour') similar to depressive symptoms in humans. Cytokine treatment of certain tumours and chronic hepatitis can also cause depressive symptoms. The prevalence of depression in patients with autoimmune diseases is higher than in the general population. Etanercept had a favourable effect on the depressive symptoms in patients with psoriasis, independent of improvement of physical symptoms. Cytokines affect the hypothalamus-pituitary-adrenal axis and cerebral neurotransmitter systems, both of which are thought to be involved in depression. Immune activation has been associated with depression, and several anti-depressive treatments affect immune parameters, although inconsistently. Since the aging process is associated with a dysregulation of the immune system, the inflammation hypothesis might be particularly true in late-life depression.


Assuntos
Envelhecimento/psicologia , Antidepressivos/uso terapêutico , Transtorno Depressivo/imunologia , Sistema Imunitário/fisiologia , Imunoterapia/psicologia , Psiconeuroimunologia , Afeto/efeitos dos fármacos , Idoso , Envelhecimento/fisiologia , Animais , Citocinas/biossíntese , Transtorno Depressivo/etiologia , Transtorno Depressivo/psicologia , Feminino , Humanos , Sistema Hipotálamo-Hipofisário/fisiologia , Masculino , Sistema Hipófise-Suprarrenal/fisiologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...