Estrogen, the Cerebrovascular System, and Dementia

Yang, Sharon X. C.; Kuchel, George A.

doi:10.1385/1-59259-824-2:099

Cited by 2 publications

(4 citation statements)

References 113 publications

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“…Similarly, a lack of estrogen could contribute to the progression of DU. Estrogens promote the survival of smooth muscle cells and neurons 56 . Ultrastructural changes described with DU 57 and other changes associated with “normative” human aging 45 have also been noted in bladders from ovariectomized rats (Table 2).…”

Section: Pathophysiologymentioning

confidence: 87%

Detrusor Underactivity: Clinical Features and Pathogenesis of an Underdiagnosed Geriatric Condition

Taylor

Kuchel

2006

J American Geriatrics Society

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191

137

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Urinary incontinence and other lower urinary tract symptoms exert a major influence on the health and independence of frail older people. Detrusor underactivity (DU) is defined as a contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span. DU may influence the clinical presentation and impede the therapy of disorders as common and as disparate as detrusor overactivity, urinary retention, and benign prostatic hyperplasia. Urodynamically, nearly two-thirds of incontinent nursing home residents exhibit DU. The clinical diagnosis of DU when present alone or in association with other bladder conditions such as detrusor overactivity (detrusor hyperactivity with impaired contractility (DHIC)) is challenging, because symptoms lack adequate precision. A catheterized and increasingly noninvasive ultrasound-based postvoid residual assessment allows a bedside diagnosis of retention and may suggest the presence of DU in individuals (mostly women) with a low likelihood of bladder outlet obstruction (BOO). Nevertheless, it cannot differentiate primary DU from retention secondary to BOO. The management of individuals with DHIC remains unsatisfactory, because antispasmodic anticholinergic medications may worsen retention, whereas bethanechol does not improve bladder emptying. Human detrusor biopsies reveal axonal degeneration, muscle loss, and fibrosis in DU. Animal studies suggest that multiple risk factors, including retention itself, lack of estrogen, infection, inflammation, and aging, may contribute to DU. Priority areas for future research include efforts to facilitate clinical nonurodynamic diagnosis of probable DU plus translational research designed to address the pathogenesis of this complex multifactorial geriatric syndrome.

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Section: Pathophysiologymentioning

confidence: 87%

Detrusor Underactivity: Clinical Features and Pathogenesis of an Underdiagnosed Geriatric Condition

Taylor

Kuchel

2006

J American Geriatrics Society

Self Cite

191

137

View full text Add to dashboard Cite

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“…There is evidence to suggest that declines in ovarian function may lead to increases in pro-inflammatory cytokines such as IL-1, IL-6 and TNF-a (Yang and Kuchel, 2004). These changes are very subtle compared to the larger increases associated with inflammatory states (Cohen and Cohen, 1996;Cohen et al, 2003).…”

Section: Estrogen Deficiency States and Inflammationmentioning

confidence: 99%

“…These changes are very subtle compared to the larger increases associated with inflammatory states (Cohen and Cohen, 1996;Cohen et al, 2003). Interactions at the molecular level between estrogen and pro-inflammatory cytokines are highly complex and care must be taken in extrapolating even robust in vitro phenomena to physiologically meaningful results (Yang and Kuchel, 2004). However, a growing body of research points to several distinct mechanisms by which estrogen deficiency enhances the function of key pro-inflammatory pathways (Yang and Kuchel, 2004).…”

Section: Estrogen Deficiency States and Inflammationmentioning

confidence: 99%

“…Interactions at the molecular level between estrogen and pro-inflammatory cytokines are highly complex and care must be taken in extrapolating even robust in vitro phenomena to physiologically meaningful results (Yang and Kuchel, 2004). However, a growing body of research points to several distinct mechanisms by which estrogen deficiency enhances the function of key pro-inflammatory pathways (Yang and Kuchel, 2004). For example, estrogen deficiency has been shown to enhance the cell response to some cytokines by up-regulating receptor numbers and cofactors required for cytokine signal transduction and cellular action (Lin et al, 1997).…”

Section: Estrogen Deficiency States and Inflammationmentioning

confidence: 99%

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