Reduced frontal perfusion in depressed postmenopausal women: A SPECT study with WCST

Yao, Wei Jen; Pan, Hsien An; Yang, Yen Kuang; Chou, Yuan Hwa; Wang, Shan Tair; Yu, Chin Yin; Lin, Hong

doi:10.1016/j.maturitas.2007.09.014

Cited by 8 publications

(6 citation statements)

References 29 publications

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“…However, chronic stress consistently results in dysregulation of mPFC layer V subcortical targets such as the hypothalamus and amygdala (Beyer et al, 2000, Shelton, 2000, Shin et al, 2005, Yao et al, 2008), suggesting a stress-induced impairment of mPFC top-down regulation. However, the effects of chronic restraint stress (CRS) on layer V mPFC neurons are unknown.…”

Section: Introductionmentioning

confidence: 99%

Structural and functional alterations to rat medial prefrontal cortex following chronic restraint stress and recovery

et al. 2009

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Chronic stress has been shown in animal models to result in altered dendritic morphology of pyramidal neurons of the medial prefrontal cortex (mPFC). It has been hypothesized that the stress-induced dendritic retractions and spine loss lead to disrupted connectivity that results in stress-induced functional impairment of mPFC. While these alterations were initially viewed as a neurodegenerative event, it has recently been established that stress induced dendritic alterations are reversible if animals are given time to recover from chronic stress. However, whether spine growth accompanies dendritic extension remains to be demonstrated. It is also not known if recovery-phase dendritic extension allows for re-establishment of functional capacity. The goal of this study, therefore, was to characterize the structural and functional effects of chronic stress and recovery on the infralimbic (IL) region of the rat mPFC. We compared neuronal morphology of layer V IL pyramidal neurons from animals subjected to 21 days of chronic restraint stress (CRS) to those that experienced CRS followed by a 21 day recovery period. Layer V pyramidal cell functional capacity was assessed by intra-IL long-term potentiation (LTP) both in the absence and presence of SKF38393, a dopamine receptor partial agonist and a known PFC LTP modulator. We found that stress-induced IL apical dendritic retraction and spine loss co-occur with receptor-mediated impairments to catecholaminergic facilitation of synaptic plasticity. We also found that while post-stress recovery did not reverse distal dendritic retraction, it did result in over-extension of proximal dendritic neuroarchitecture and spine growth as well as a full reversal of CRS-induced impairments to catecholaminergic-mediated synaptic plasticity. Our results support the hypothesis that disease-related PFC dysfunction is a consequence of network disruption secondary to altered structural and functional plasticity and that circuitry reestablishment may underlie elements of recovery. Accordingly, we believe that pharmacological treatments targeted at preventing dendritic retraction and spine loss or encouraging circuitry reestablishment and stabilization may be advantageous in the prevention and treatment of mood and anxiety disorders.

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Section: Introductionmentioning

confidence: 99%

Structural and functional alterations to rat medial prefrontal cortex following chronic restraint stress and recovery

et al. 2009

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“…In a previous study (Yao et al, 2008), we showed a decrease in frontal CBF in depressed postmenopausal women. In this study, we investigated whether HRT improves frontal CBF, mood, and cognitive function in depressed postmenopausal women and, if so, how such improvements are related.…”

Section: Introductionmentioning

confidence: 56%

Frontal Cerebral Blood Flow Changes after Hormone Replacement Therapy in Depressed Postmenopausal Women

Yao

Pan

Wang

et al. 2009

J Cereb Blood Flow Metab

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We investigated the effects of hormone replacement therapy (HRT) on frontal cerebral blood flow (CBF), depressive symptoms, and cognitive function in depressed postmenopausal women. Fourteen postmenopausal women with depressive symptoms underwent HRT, and seven controls not undergoing HRT were studied. We evaluated frontal CBF, expressed as frontal/cerebellum (F/C) ratio, using Tc-99m hexamethyl propylene amine oxime single photon emission computed tomography (Tc-99m HMPAO SPECT), cognitive function using the Mini-Mental Status Examination (MMSE), and depression using the HAD (Hospital Anxiety and Depression) scale. All studies were carried out at initial status and after 9 months. Single photon emission computed tomography was performed at rest and at activation during the Wisconsin Card Sorting Test (WCST). Initial frontal CBF was not different between groups. After 9 months, resting frontal CBF was similar between groups. However, activated frontal CBF was significantly higher in the HRT group than in controls (F/C ratio: 0.924±0.04 versus 0.853±0.05, P=0.007). Furthermore, the increase in the activated F/C ratio was inversely associated with years since menopause. Mini-Mental Status Examination scores improved after HRT, but depression scores did not. Hormone replacement therapy improved frontal CBF and cognitive function but not depression in postmenopausal women. The changes in frontal CBF were detected only during WCST activation and were most apparent during early postmenopausal years.

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“…One study has also shown that in cognitively intact but depressed postmenopausal women, there was no difference in basal cerebral blood flow between women with and without depression. However, the authors observed a blunted rise in cerebral blood flow during the Wisconsin Card Sorting Task (WCST; CVR to cognitive task), which correlated with poorer scores on the Mini-Mental State Examination, one measure of global cognition, but not with WCST performance [45] . Alleviating depressive symptoms early in menopause may be crucial for reducing the risk of dementia in women later in life.…”

Section: Discussionmentioning

confidence: 96%

Poor cerebrovascular function is an early marker of cognitive decline in healthy postmenopausal women

Wong

Evans

Howe

2016

A&D Transl Res & Clin Interv

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IntroductionImpairment of cerebrovascular function becomes evident after menopause. No study has yet explored relationships between deficits in cerebrovascular function, cognitive performance, and mood in postmenopausal women.MethodCerebrovascular function was assessed in 80 healthy postmenopausal women by monitoring blood flow velocity (BFV) in the middle and posterior cerebral arteries using transcranial Doppler ultrasound at rest, following a hypercapnic challenge, and during performance of a cognitive test battery; the latter assessed domains of memory and executive functions. Various measures of mood (i.e., Profile of Mood States and Center for Epidemiological Studies Depression Scale) were also assessed.ResultsCerebral artery elasticity and BFV responsiveness to cognitive tests (neurovascular coupling) correlated with cognitive performance but not with depressive symptoms or mood states. Mood deficits were related to poor cognitive performance.ConclusionThese results highlight the importance of adequate cerebral perfusion for optimized cognitive function in healthy postmenopausal women. Preventative strategies to attenuate accelerated cognitive decline should also consider restoring cerebrovascular function.

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Reduced frontal perfusion in depressed postmenopausal women: A SPECT study with WCST

Cited by 8 publications

References 29 publications

Structural and functional alterations to rat medial prefrontal cortex following chronic restraint stress and recovery

Structural and functional alterations to rat medial prefrontal cortex following chronic restraint stress and recovery

Frontal Cerebral Blood Flow Changes after Hormone Replacement Therapy in Depressed Postmenopausal Women

Poor cerebrovascular function is an early marker of cognitive decline in healthy postmenopausal women

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