Biomedical subjects

Laura McCabe

Publications and source records attributed to Laura McCabe.

6 recordsLinked to original sources

PubMed2007

Epidemiology of social phobia in later life.

OBJECTIVE: Although anxiety disorders, including social phobia (SP), are common among older adults, very little is known about the epidemiology of SP in later life. METHOD: Using data drawn from a large, nationally representative sample of older adults from Canada (N=12,792), the authors estimate lifetime and 12-month prevalence of social phobia and examine demographic predictors and patterns of comorbidity of current SP in this population. RESULTS: The results reveal that SP is a prevalent disorder in later life with lifetime and 12-month prevalence estimates of 4.94% and 1.32%, respectively. Current SP (12-month) declines with age and is more common in individuals with other psychiatric disorders. Interestingly, there is no correlation between current SP and gender, marital status, or socioeconomic status. CONCLUSIONS: SP remains a highly prevalent disorder even in late life with the pattern of feared/avoided situations being strikingly similar to that of younger populations.

Age Distribution↗

PubMed2006

Prevalence and correlates of agoraphobia in older adults.

OBJECTIVE: Agoraphobia has been previously found to be a relatively prevalent disorder in the older adult. However, little is known about the nature of this disorder in the elderly population. The purpose of this study was to identify risk factors, illness characteristics, and comorbidity of agoraphobia in the elderly. METHODS: This was a national community mental health survey that included 12,792 individuals > or = 55 years. Agoraphobia was assessed using the World Mental Health Composite International Diagnostic Interview. Social, demographic, psychiatric, and physical variables previously found to be associated with agoraphobia in the adult population were measured. Bivariate and logistic regression analyses were used to examine these associations. RESULTS: The prevalence of agoraphobia in adults over 55 was 0.61% (95% confidence interval [CI]: 0.40-0.82). In bivariate analysis, the condition was more common in the younger age groups, women, and those widowed or divorced. It was also more common in individuals with chronic health conditions and those with comorbid psychiatric disorders. However, in the multivariate model, chronic health conditions and panic disorder were no longer significant. Most cases of agoraphobia in the elderly were of early onset (age <55 years). The majority of patients with agoraphobia did not have concurrent panic disorder. CONCLUSION: Lower prevalence rates of agoraphobia in the elderly were found compared with previous studies. The degree to which this is a measurement issue is discussed. The low correlation between agoraphobia and panic disorder raises further questions about the nature and etiology of agoraphobia in the elderly. Implications for future research and clinical practice are discussed.

Adolescent↗

PubMed2004

Activation of NR1a/NR2B receptors by soluble factors from APP-stimulated monocyte-derived macrophages: implications for the pathogenesis of Alzheimer's disease.

Amyloid-beta peptide (Abeta), the major component of amyloid plaques, can activate brain mononuclear phagocytes (MP; macrophages and microglia), leading to their secretion of neurotoxins. Recent studies strongly suggest that MP-mediated neurotoxicity plays an important role in the pathogenesis of Alzheimer's disease (AD). To further explore this notion, human monocyte-derived macrophages (MDM) were stimulated with naturally secreted alpha-processing soluble amyloid precursor protein/p3 (alphaAPPs/p3) or beta-processing APP/Abeta (betaAPPs/Abeta). MDM conditioned media (MCM) was recovered and tested for its ability to activate recombinant N-methyl-d-aspartate (NMDA) receptor subtype NR1a/NR2B expressed in Xenopus oocytes. Pressure ejection of alphaAPPs/p3- and betaAPPs/Abeta-stimulated MCM produced inward currents of 59.5 +/- 8.9 nA (mean +/- S.E.M., n = 31) and 111.1 +/- 21.0 nA (n = 42) in NR1a/NR2B-expressing oocytes, respectively. The MCM-induced currents were concentration dependent and blocked by 50 microM of the NMDA receptor antagonist 2-amino-5-phosphnovalerate, but not by a non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM). The alphaAPPs/p3- and betaAPPs/Abeta-stimulated MCM placed in non-injected oocytes failed to generate inward current. These results demonstrate that APPs/Abeta-stimulated MCM directly activate NMDA receptor subtypes relevant in the pathogenesis of AD.

Alzheimer Disease↗

PubMed2004

Residential crisis units. Are we missing out on a good idea?

Residential Crisis Units (RCU) are non-hospital-based facilities that provide mental health crisis intervention. This paper reviews the RCU literature base and finds good evidence of the ability of RCUs to function as alternatives to hospitalization for many consumers, with equivalent effectiveness and for significantly less cost. Despite this promising research, the RCU model has not been widely adopted. Using two crisis units as case examples as well as key informant interviews, this paper explores factors affecting the lack of dissemination and potential barriers to the growth of the RCU model.

Canada↗

PubMed2003

Activation of NR1a/NR2B receptors by monocyte-derived macrophage secretory products: implications for human immunodeficiency virus type one-associated dementia.

The final pathways for neuronal injury in human immunodeficiency virus type one (HIV-1)-associated dementia (HAD) were investigated in Xenopus oocytes expressing recombinant NR1a/NR2B N-methyl-D-aspartate (NMDA) receptors exposed to secretory products from HIV-infected macrophages. Pressure ejection of HIV-1-infected and CD40 ligand-stimulated human monocyte-derived macrophage (MDM) fluids produced inward currents in oocytes expressing NR1a/NR2B (30.2+/-5.1 nA, n=42, mean+/-SE), but not in uninjected cells. In contrast, control (uninfected MDM) fluids induced currents of 4.5+/-0.5 nA (n=17). Infected or stimulated MDM without virus showed intermediate responses. The induced currents were MDM fluid dose-dependent and blocked by the NMDA receptor antagonist 2-amino-5-phosphonovalerate (50 microM), but not by 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM). Although low levels of glutamate were detected in the culture fluids, the addition of L-glutamate decarboxylase to the MDM did not significantly change the level of induced inward currents. Our experiments demonstrate that secretory factors from HIV-1-infected MDM activate NMDA receptors NR1a/NR2B and may contribute to neuronal demise during HAD.

AIDS Dementia Complex↗

PubMed2003

Amyloid precursor protein-processing products affect mononuclear phagocyte activation: pathways for sAPP- and Abeta-mediated neurotoxicity.

Increasing evidence strongly supports the role of glial immunity in the pathogenesis of Alzheimer's disease (AD). To investigate such events we have developed cell systems mimicking the interactions between beta-amyloid precursor protein (APP)-expressing neurons and brain mononuclear phagocytes (MP; macrophages and microglia). MP were co-cultured with neuronal cells expressing wild type APP or familial AD-linked APP mutants. The latter was derived from recombinant adenoviral constructs. Neuronal APP processing products induced MP activation, reactive oxygen species, and neurotoxic activities. These occurred without the addition of pro-inflammatory cytokines and were reversed by depletion of amyloid beta-peptide (Abeta) and secreted APP (sAPP). Neurotoxic activities were diminished by superoxide dismutase mimetics and NMDA receptor inhibitors. Microglial glutamate secretion was suppressed by the cystine-glutamate antiporter inhibitor and its levels paralleled the depletion of sAPP and Abeta from conditioned media prepared from APP-expressing neurons. The excitotoxins from activated MP were potent enough to evoke recombinant NMDA receptor-mediated inward currents expressed in vitro in the Xenopus oocytes. These results demonstrate that neuronal APP-processing products can induce oxidative neurotoxicity through microglial activation.

Amino Acid Transport System y+↗