Objective: Caregivers of individuals with Alzheimer's disease and related dementias (ADRD) often experience debilitating caregiver burden and emotional distress. To address these negative emotional consequences of caregiving, we will test and refine a strategy training intervention - Problem-Solving Training (PST) - that promotes self-efficacy and reduces caregiver burden and depressive symptoms. Previous research supports efficacy of PST; however, we do not know exactly how many PST sessions are needed or if post-training "boosters" are required to maintain PST benefits.
View Article and Find Full Text PDFBackground: Cerebral edema peaks 36-72 h after moderate traumatic brain injury but thought to be uncommon after mild traumatic brain injury. Post-traumatic headache can develop 48-72 h post-injury, perhaps reflecting the developing cerebral edema. Pseudotumor cerebri can result from various causes, including cerebral edema, and is characterized by increased intracranial pressure, headache, visual, and other common symptoms.
View Article and Find Full Text PDFPurpose: On arrival to the postanesthesia care unit (PACU), patients are observed closely for significant neurological status changes. In particular, patients require frequent neurological examinations, which include assessment of the pupils for changes and/or abnormalities.
Design: This is a prospective, nonrandomized, observational study to examine the findings of pupillary examinations by nurses using different light sources in patients with existing pupillary assessments as ordered by standard of care.
Objective: We hypothesized that nurses would benefit from the fellowship model traditionally used to engage physicians in clinical research. The Neuroscience Nursing Research Center (NNRC) fellowship program was created as a model for engaging nurses at all levels of clinical practice to become active in clinical research.
Background: The NNRC was established in 2013 as a novel approach to promote bedside nurses as primary investigators in clinical research.
Nurses caring for patients with acute stroke are likely to administer both music and medication with therapeutic intent. The administration of medication is based on accumulated scientific evidence and tailored to the needs of each patient. However, the therapeutic use of music is generally based on good intentions and anecdotal evidence.
View Article and Find Full Text PDFIntroduction: The emergency department (ED) is demanding and high risk. The impact of sleep quantity has been hypothesized to impact patient care. This study investigated the hypothesis that fatigue and impaired mentation, due to sleep disturbance and shortened overall sleeping hours, would lead to increased nursing errors.
View Article and Find Full Text PDFChannels (Austin)
June 2015
Dysregulated endoplasmic reticulum (ER) calcium (Ca(2+)) signaling is reported to play an important role in Alzheimer disease (AD) pathogenesis. The role of ER Ca(2+) release channels, the ryanodine receptors (RyanRs), has been extensivelys tudied in AD models and RyanR expression and activity are upregulated in the brains of various familial AD (FAD) models.The objective of this study was to utilize a genetic approach to evaluate the importance of RyanR type 3 (RyanR3) in the context of AD pathology.
View Article and Find Full Text PDFMol Neurodegener
November 2011
Background: Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a polyglutamine expansion in the Huntingtin protein which results in the selective degeneration of striatal medium spiny neurons (MSNs). Our group has previously demonstrated that calcium (Ca2+) signaling is abnormal in MSNs from the yeast artificial chromosome transgenic mouse model of HD (YAC128). Moreover, we demonstrated that deranged intracellular Ca2+ signaling sensitizes YAC128 MSNs to glutamate-induced excitotoxicity when compared to wild type (WT) MSNs.
View Article and Find Full Text PDFPolyglutamine(polyQ)-expanded proteins are potential therapeutic targets for the treatment of polyQ expansion disorders such as Huntington's disease (HD) and spinocerebellar ataxia type 3 (SCA3). Here, we used an amino-terminal fragment of a mutant Huntingtin protein (Htt-N-82Q) as bait in an unbiased screen of a 60,000 peptoid library. Peptoid HQP09 was selected from the isolated hits and confirmed as a specific ligand of Htt-N-82Q and Atxn3-77Q mutant proteins in biochemical experiments.
View Article and Find Full Text PDFSci China Life Sci
August 2011
Alzheimer disease (AD) is the most common neurodegenerative disorder worldwide and is at present, incurable. The accumulation of toxic amyloid-beta (Aβ) peptide aggregates in AD brain is thought to trigger the extensive synaptic loss and neurodegeneration linked to cognitive decline, an idea that underlies the 'amyloid hypothesis' of AD etiology in both the familal (FAD) and sporadic forms of the disease. Genetic mutations causing FAD also result in the dysregulation of neuronal calcium (Ca(2+)) handling and may contribute to AD pathogenesis, an idea termed the 'calcium hypothesis' of AD.
View Article and Find Full Text PDFCell Calcium
September 2011
Alzheimer's disease (AD) is the most common neurodegenerative disorder worldwide and is at present, incurable. The accumulation of toxic amyloid-beta (Aβ) peptide aggregates in AD brain is thought to trigger the extensive synaptic loss and neurodegeneration linked to cognitive decline, an idea that underlies the 'amyloid hypothesis' of AD etiology in both the familal (FAD) and sporadic forms of the disease. Genetic mutations causing FAD also result in the dysregulation of neuronal calcium (Ca(2+)) handling and may contribute to AD pathogenesis, an idea termed the 'calcium hypothesis' of AD.
View Article and Find Full Text PDFMissense mutations in presenilin 1 (PS1) and presenilin 2 (PS2) proteins are a major cause of familial Alzheimer disease. Presenilins are proteins with nine transmembrane (TM) domains that function as catalytic subunits of the γ-secretase complex responsible for the cleavage of the amyloid precursor protein and other type I transmembrane proteins. The water-filled cavity within presenilin is necessary to mediate the intramembrane proteolysis reaction.
View Article and Find Full Text PDFMutations in presenilins 1 and 2 (PS1 and PS2) are responsible for approximately 40% of all early onset familial Alzheimer's disease (FAD) monogenic cases. Presenilins (PSs) function as the catalytic subunit of γ-secretase and support cleavage of the amyloid-β protein precursor (AβPP). We previously discovered that PSs also function as passive endoplasmic reticulum (ER) calcium (Ca2+) leak channels and that most FAD mutations in PSs affected their ER Ca2+ leak function.
View Article and Find Full Text PDFJ Alzheimers Dis
September 2010
Alzheimer's disease (AD) is the most common neurodegenerative disorder among the aged worldwide. AD is characterized by extensive synaptic and neuronal loss that leads to impaired memory and cognitive decline. The cause of AD is not completely understood and no effective therapy has been developed.
View Article and Find Full Text PDFAlzheimer disease (AD) is the most common neurodegenerative disorder worldwide and is at present, incurable. The accumulation of toxic amyloid-beta (Abeta) peptide aggregates in AD brain are thought to trigger the extensive synaptic loss and neurodegeneration linked to cognitive decline, an idea that underlies the 'amyloid hypothesis' of AD etiology in both the familal (FAD) and sporadic forms of the disease. Mutations causing FAD also result in the dysregulation of neuronal calcium (Ca2+) handling and may contribute to AD pathogenesis, an idea termed the 'calcium hypothesis' of AD.
View Article and Find Full Text PDFThe cellular pathology of Alzheimer's disease is progressive and protracted leading eventually to considerable neuronal death. The underlying mechanisms of the pathology are complex but changes in the control of intracellular Ca2+ are believed to contribute to the demise of neurons. In this study, we investigated the functional consequences of an increase in the expression of the type 3 isoform of the ryanodine receptor (RyR3).
View Article and Find Full Text PDFDisruption of intracellular calcium homeostasis precedes the neurodegeneration that occurs in Alzheimer disease (AD). Of the many neuronal calcium-regulating proteins, we focused on endoplasmic reticulum (ER)-resident ryanodine receptors (RyRs) because they are increased in the hippocampus of mice expressing mutant presenilin-1 and are associated with neurotoxicity. Others have observed that ryanodine binding is elevated in human postmortem hippocampal regions suggesting that RyR(s) are involved in AD pathogenesis.
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