As a social identity anchored in a system of guiding beliefs and symbols, religion ought to serve a uniquely powerful function in shaping psychological and social processes. Religious identification offers a distinctive "sacred" worldview and "eternal" group membership, unmatched by identification with other social groups. Thus, religiosity might be explained, at least partially, by the marked cognitive and emotional value that religious group membership provides. The uniqueness of a positive social group, grounded in a belief system that offers epistemological and ontological certainty, lends religious identity a twofold advantage for the promotion of well-being. However, that uniqueness may have equally negative impacts when religious identity itself is threatened through intergroup conflict. Such consequences are illustrated by an examination of identities ranging from religious fundamentalism to atheism. Consideration of religion's dual function as a social identity and a belief system may facilitate greater understanding of the variability in its importance across individuals and groups.

Mutations of the DJ-1 (PARK7) gene are linked to familial Parkinson's disease. We used gene targeting to generate DJ-1-deficient mice that were viable, fertile, and showed no gross anatomical or neuronal abnormalities. Dopaminergic neuron numbers in the substantia nigra and fiber densities and dopamine levels in the striatum were normal. However, DJ-1؊͞؊ mice showed hypolocomotion when subjected to amphetamine challenge and increased striatal denervation and dopaminergic neuron loss induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine. DJ-1؊͞؊ embryonic cortical neurons showed increased sensitivity to oxidative, but not nonoxidative, insults. Restoration of DJ-1 expression to DJ-1؊͞؊ mice or cells via adenoviral vector delivery mitigated all phenotypes. WT mice that received adenoviral delivery of DJ-1 resisted 1-methyl-4-phenyl-1,2,3,6-tetrahydropyrindine-induced striatal damage, and neurons overexpressing DJ-1 were protected from oxidative stress in vitro. Thus, DJ-1 protects against neuronal oxidative stress, and loss of DJ-1 may lead to Parkinson's disease by conferring hypersensitivity to dopaminergic insults. P arkinson's disease (PD) is a neurodegenerative disorder characterized by tremor, rigidity, akinesia, and postural instability (1). The cause of PD remains unknown, but epidemiological and genetic studies have suggested that the observed loss of dopaminergic neurons in PD is due to defects in common intracellular signaling pathways (2). Genes linked to familial PD include ␣-synuclein (3), Parkin (4), UCH-L1 (5), PINK1 (6), and dardarin (7). Proteins encoded by these genes are thought to be involved in protein aggregation and proteasome function, processes which, when disrupted in model systems, can also result in noninherited forms of PD (8). Recently, loss-of-function mutations in the DJ-1 locus were found in families with autosomal recessive early-onset PD (9). Additional studies have confirmed other DJ-1 mutations in various PD cohorts (10). DJ-1 was initially cloned as a putative oncogene (11) and as part of an RNA-binding complex (12). DJ-1 is highly expressed by normal astrocytes (13) and has been implicated in fertilization (14) and tumorigenesis (15,16). Studies of the crystal structure of DJ-1 (17) suggest that a particular DJ-1 mutation (L166P) reduces DJ-1 protein stability (18)(19)(20), resulting in degradation through the ubiquitin-proteasome system (21, 22). However, the physiological function of DJ-1 remains largely unknown.Motor impairments in PD patients result from inhibition of the nigrostriatal motor pathway. This inhibition is due to the loss of dopaminergic neurons in the substantia nigra pars compacta (SNc) (8). The cause of the dopaminergic neuron loss remains unknown, but oxidative stress leading to apoptotic neuronal death has been implicated (23). Various neurotoxic paradigms have been studied in an effort to reproduce oxidative stress leading to neuronal loss in the SNc. Of these, administration of the well characterized meperidine analogue 1-methyl-4-phenyl-1,2,3,6-te...

Early-life stimulation (e.g., brief handling) attenuates the behavioral and neuroendocrine responses to stressors encountered in adulthood, particularly with respect to activation of hypothalamic-pituitary-adrenal (HPA) activity. In contrast, if neonates were subjected to a more severe stressor, such as protracted separation from the dam or exposure to an endotoxin, then the adult response to a stressor was exaggerated. These early-life experiences program HPA functioning, including negative feedback derived from stimulation of hippocampal glucocorticoid receptors, and corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) coexpression in PVN neurons, to modify the response to subsequent stressor experiences. The persistent variations of HPA activity observed in handled/stimulated animals may stem from alterations in dam-pup interactions (e.g. increased arched-back feeding, licking, grooming). In addition genetic makeup is critical in determining stress reactivity. For instance, BALB/cByJ mice are more reactive to stressors than C57BL/6ByJ mice, exhibiting greater HPA hormonal alterations and behavioral disturbances. BALB/cByJ also fail to acquire a spatial learning response in a Morris water-maze paradigm, which has been shown to be correlated with hippocampal cell loss associated with aging. Early-life handling of BALB/cByJ mice prevented these performance deficits and attenuated the hypersecretion of ACTH and corticosterone elicited by stressors. The stressor reactivity may have been related to maternal and genetic factors. When BALB/cByJ mice were raised by a C57BL/6ByJ dam, the excessive stress-elicited HPA activity was reduced, as were the behavioral impairments. However, cross-fostering the more resilient C57BL/6ByJ mice to a BALB/cByJ dam failed to elicit the behavioral disturbances. It is suggested that genetic factors may influence dam-pup interactive styles and may thus proactively influence the response to subsequent stressors among vulnerable animals. In contrast, in relatively hardy animals the early-life manipulations may have less obvious effects.

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The current paper reviews research that has explored the intergenerational effects of the Indian Residential School (IRS) system in Canada, in which Aboriginal children were forced to live at schools where various forms of neglect and abuse were common. Intergenerational IRS trauma continues to undermine the well-being of today’s Aboriginal population, and having a familial history of IRS attendance has also been linked with more frequent contemporary stressor experiences and relatively greater effects of stressors on well-being. It is also suggested that familial IRS attendance across several generations within a family appears to have cumulative effects. Together, these findings provide empirical support for the concept of historical trauma, which takes the perspective that the consequences of numerous and sustained attacks against a group may accumulate over generations and interact with proximal stressors to undermine collective well-being. As much as historical trauma might be linked to pathology, it is not possible to go back in time to assess how previous traumas endured by Aboriginal peoples might be related to subsequent responses to IRS trauma. Nonetheless, the currently available research demonstrating the intergenerational effects of IRSs provides support for the enduring negative consequences of these experiences and the role of historical trauma in contributing to present day disparities in well-being.

What is already known on this subject? It has been established that the public is often confused by the threat that a potential pandemic virus poses and that they are unsure of what information related to the disease they can trust. Government health agencies often walk the line of minimizing the threat to prevent panic, but simultaneously emphasize the importance of action (vaccination) to prevent a worldwide pandemic. What does this study add? Beyond the physical threat of a pandemic, a significant psychological toll may occur for certain individuals. Anxiety regarding H1N1 is heightened amongst those who cannot tolerate uncertainty. Appraisals of threat, control, and the use of emotion-focused coping mediate the above relationship.

Recent evidence indicates that cyclin-dependent kinases (CDKs, cdks) may be inappropriately activated in several neurodegenerative conditions. Here, we report that cdk5 expression and activity are elevated after administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin that damages the nigrostriatal dopaminergic pathway. Supporting the pathogenic significance of the cdk5 alterations are the findings that the general cdk inhibitor, flavopiridol, or expression of dominant-negative cdk5, and to a lesser extent dominant-negative cdk2, attenuates the loss of dopaminergic neurons caused by MPTP. In addition, CDK inhibition strategies attenuate MPTP-induced hypolocomotion and markers of striatal function independent of striatal dopamine. We propose that cdk5 is a key regulator in the degeneration of dopaminergic neurons in Parkinson's disease.1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine ͉ neurodegeneration P arkinson's disease (PD) is a neurodegenerative disorder characterized by disabling motor abnormalities, including tremor, muscle rigidity, paucity of voluntary movements, and postural instability (1). In several mammalian species, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces most of the biochemical and pathological alterations seen in PD, including the loss of dopaminergic neurons of the substantia nigra pars compacta (SNc) (1). Current treatment strategies for PD consist primarily of dopamine replacement therapy with levodopa or dopamine agonists (1). Although effective in the early stages of the disease, chronic dopamine replacement therapy can cause debilitating side effects. Accordingly, concerted research efforts have been focused on developing neuroprotective strategies that will halt or slow the progression of PD.Recent evidence implicates cyclin-dependent kinases (CDKs) in the pathogenesis of several neurodegenerative disorders. CDKs are serine͞threonine kinases best characterized for their role in cell cycle progression. To be active, CDKs require binding to specific regulatory partners such as cyclins (2). Up-regulation of a variety of cell cycle-related CDKs and͞or cyclins has been reported in a number of in vitro neuronal death paradigms (3-8).The importance of such observations is substantiated by reports that inappropriate activation of cell cycle-related pathways has been correlated with the pathogenesis of stroke (9, 10) and Alzheimer's disease (11). However, the identity and functional requirement of individual CDK members in neurodegeneration remain to be elucidated.In contrast to the mitotic CDKs, cdk5 activity is predominantly, although not exclusively, associated with postmitotic neurons (12). cdk5 activation requires association with its regulatory partner, p35 (13) or p39 (14). The p35͞cdk5 complex is required for proper development of the central nervous system (15, 16), process outgrowth (17), axonal migration (18, 19), cortical lamination (16, 20), cell adhesion (20), axonal transport (21), and synaptic activity (22). Just as with cell cycle-related CDK...

As numerous coping strategies to deal with stressors can be used concurrently or sequentially, it may be productive to consider coping from a broad, systemic perspective. Using profile analysis and multivariate techniques, we demonstrated that coping profiles comprising multiple strategies distinguished between various mood states (dysphoria, anxiety, major depression, dysthymia and obsessive-compulsive disorder (OCD)). Generally, affective disturbances were associated with increased levels of rumination, cognitive distraction and emotion-focused coping (emotional expression, other-blame, self-blame, emotional containment and passive resignation) coupled with diminished problem solving and social support seeking. These coping profiles, however, varied as a function of anxiety vs. dysphoria, and severity of dysphoric symptoms, although the profile of dysphoric individuals was similar to that of clinically diagnosed dysthymic and major depressive patients. While coping profiles were generally stable over time (6 months), improvement or deterioration of mood was accompanied by corresponding alterations of coping profiles. Importantly, coping profile was not simply a correlate of dysphoric mood, but was also found to be an antecedent condition that favored the evolution of more severe affective problems. It is suggested that a multidimensional approach may prove useful in understanding coping as a dynamic system, and may have implications for clinical intervention.