Publications by authors named "Roxanne Sterniczuk"

The mammalian circadian clock in the suprachiasmatic nucleus (SCN) is a heterogeneous structure. Two key populations of cells that receive retinal input and are believed to participate in circadian responses to light are cells that contain vasoactive intestinal polypeptide (VIP) and gastrin-releasing peptide (GRP). VIP acts primarily through the VPAC2 receptor, while GRP works primarily through the BB2 receptor.

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Background: Even subtle impairments on cognitive test scores can be associated with future cognitive decline and dementia. We assayed the relationships between test score impairment and adverse outcomes.

Methods: Secondary analyses were performed on data from non-institutionalized participants, 50+ years of age (N = 30,038), from 12 countries taking part in the Survey of Health, Ageing and Retirement in Europe (SHARE) longitudinal study on aging.

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Maintaining a stable and adequate sleeping pattern is associated with good health and disease prevention. As a restorative process, sleep is important for supporting immune function and aiding the body in healing and recovery. Aging is associated with characteristic changes to sleep quantity and quality, which make it more difficult to adjust sleep-wake rhythms to changing environmental conditions.

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Daily photic resetting of the circadian system relies on the transmission of light information from the retina to retinorecipient cells within the ventrolateral suprachiasmatic nucleus (SCN) core, and subsequent activation of rhythmic clock cells in the dorsolateral region. Some neurochemicals such as gastrin-releasing peptide (GRP) mimic the phase shifting effects of light and induce Ca(2+)-dependent gene expression in the SCN. Activation of the cAMP-response element binding protein (CREB) is necessary for Ca(2+)-dependent transcription to occur and accompanies behavioral phase shifting; however, several biochemical cascades are involved in this phenomenon.

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People with Alzheimer' s disease (AD) commonly complain of sleep disturbances, which are seen in a wide variety of conditions that become more common in late life. It is not known whether sleep-related symptoms are associated with AD independently of their association with other illnesses. Secondary analyses of sleep-related measures collected through the Survey of Health, Ageing and Retirement in Europe (SHARE; i.

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Alzheimer's disease (AD) is characterized by distinct behavioral and cognitive deficits that differ from those observed in normal aging. Transgenic models of AD are a promising tool in understanding the underlying mechanisms and cause of disease. The triple-transgenic mouse model of AD (3xTg-AD) is the only model to exhibit both Abeta and tau pathology that is characteristic of the human form.

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Circadian disturbances, including a fragmented sleep-wake pattern and sundowning, are commonly reported early in the progression of Alzheimer's disease (AD). These changes are distinctly different from those observed in non-pathological aging. Transgenic models of AD are a promising tool in understanding the underlying mechanisms and cause of disease.

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Circadian rhythms in physiological, endocrine and metabolic functioning are controlled by a neural clock located in the suprachiasmatic nucleus (SCN). This structure is endogenously rhythmic and the phase of this rhythm can be reset by light information from the eye. A key feature of the SCN is that while it is a small structure containing on the order of about 20,000 cells, it is amazingly heterogeneous.

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The suprachiasmatic nucleus (SCN) contains the master mammalian circadian pacemaker. It is comprised of several phenotypically distinct cell groups, some of which are situated in the weakly rhythmic retinoresponsive ventrolateral region while others are found in the rhythmic, non-retinoresponsive dorsomedial region. The mechanism by which retinorecipient cells convey photic information to the dorsomedial clock cells is unclear.

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The master circadian clock, located in the suprachiasmatic nucleus (SCN), is synchronized to the external world primarily through exposure to light. A second class of stimuli based on arousal or activity can also reset the hamster circadian clock in a manner distinct from light. The mechanism underlying these non-photic phase shifts is unknown, although suppression of canonical clock genes and immediate early genes has been implicated.

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Circadian rhythms can be reset by both photic and non-photic stimuli. Recent studies have used long light exposure to produce photic phase shifts or to enhance non-photic phase shifts. The presence or absence of light can also influence the expression of locomotor rhythms through masking; light during the night attenuates locomotor activity, while darkness during the day induces locomotor activity in nocturnal animals.

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The relationship between monthly alcohol consumption over the past 6 months and facial symmetry perception ability was examined in young sober women with typical college-age drinking patterns. Facial symmetry detection performance was inversely related to typical monthly alcohol consumption, r (41) = -0.57, p < 0.

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