Contexte : le lien entre maladie mentale et radicalisation n’a pas encore été établi et peu d’études ont examiné ce lien. Certaines études suggèrent que la maladie mentale peut prédisposer les individus à développer des croyances extrémistes et des comportements violents, d’autres études suggèrent le contraire. Cela soulève deux questions fondamentales : 1) Existe-t-il un lien entre santé mentale et extrémisme violent ? 2) Qui commet ce type d’actes violents ? Les auteurs explorent ici les facteurs qui prédisposent les individus à développer des conceptions extrémistes avec un accent particulier sur les combattants islamiques et s’il existe un lien avec la maladie mentale dans ces groupes. Méthode : les auteurs ont procédé à une revue de la littérature sur la relation entre maladie mentale et radicalisation violente pour dégager un consensus sur ce sujet. Ils ont effectué des recherches documentaires sur le site web du Centre national d’information sur la biotechnologie, en utilisant les mots clés « violent extremism » (extrémisme violent) et (santé mentale). Résultat : la recherche électronique a proposé 38 articles, et seulement 12 remplissaient les critères de sélection. Ces articles ont exploré les problèmes de maladie mentale et de radicalisation violente. Ces études ont mis en évidence trois conclusions principales : 1) Il n’y a pas de lien entre maladie mentale et radicalisation violente, une telle radicalisation peut même servir de facteur de protection contre dépression et symptômes d’anxiété ; 2) Le comportement antisocial, la délinquance, une faible estime de soi sont parmi les facteurs contributifs ; 3) Il existe de nombreux parallèles entre les individus qui se livrent à des violences à caractère religieux ou politique et les meurtriers de masse ou « loup solitaire ». Conclusion : il est nécessaire de poursuivre les recherches sur la radicalisation et la maladie mentale pour élaborer des stratégies efficaces de prévention de la menace sécuritaire et empêcher des personnes en difficulté de commettre de tels actes extrémistes ou terroristes violents. Les comportements agressifs et impulsifs, les traits narcissiques et antisociaux, la faible estime de soi et une vision du monde plutôt schizoïde semblent être associés à la radicalisation violente.

Background: In Alzheimer’s disease, growing evidence has shown that uncontrolled glial activation and neuroinflammation may contribute independently to neurodegeneration. Antiinflammatory strategies might provide benefits for this devastating disease. The aims of the present study are to address the issue of whether glial activation and proinflammatory cytokine increases could be modulated by quetiapine in vivo and in vitro and to explore the underlying mechanism. Methods: Four-month–old amyloid precursor protein (APP) and presenilin 1 (PS1) transgenic and nontransgenic mice were treated with quetiapine (5mg/kg/d) in drinking water for 8 months. Animal behaviors, total Aβ levels, and glial activation were evaluated by behavioral tests, enzyme-linked immunosorbent assay, immunohistochemistry, and Western blot accordingly. Inflammatory cytokines and the nuclear factor kappa B pathway were analyzed in vivo and in vitro. Results: Quetiapine improves behavioral performance, marginally affects total Aβ40 and Aβ42 levels, attenuates glial activation, and reduces proinflammatory cytokines in APP/PS1 mice. Quetiapine suppresses Aβ1-42-induced activation of primary microglia by decresing proinflammatory cytokines. Quetiapine inhibits the activation of nuclear factor kappa B p65 pathway in both transgenic mice and primary microglia stimulated by Aβ1–42. Conclusions: The antiinflammatory effects of quetiapine in Alzheimer’s disease may be involved in the nuclear factor kappa B pathway. Quetiapine may be an efficacious and promising treatment for Alzheimer’s disease targeting on neuroinflammation.

Quetiapine, an atypical antipsychotic drug, is effective in treating the behavioral and psychological symptoms in Alzheimer's disease (AD). However, it is presently unclear whether quetiapine has beneficial effects on memory and whether the effects of quetiapine on psychological symptoms are associated with its effect on memory in AD. The present study was designed to examine the effect of chronic administration of quetiapine on the conditioned (generalized) anxiety that is related to learning experience of open arm exposure in the elevated T-maze (ETM) test in an amyloid precursor protein (APP)/presenilin 1 (PS1) double transgenic mouse model of AD. In a 2nd experiment, the effect of quetiapine on memory per se was investigated in a Y-maze test in AD mice. Non-transgenic and transgenic mice were treated with quetiapine in drinking water from the age of 2 months. After continuous treatment with quetiapine (5 mg/kg/day) for 10 months, mice were tested for conditioned anxiety on the ETM task. After ETM testing, the expression of brain-derived neurotrophic factor (BDNF), a neuroprotective protein, was examined by immunohistochemistry in the basolateral amygdala (BLA) and hippocampus. In the 2nd experiment, the effect of quetiapine (2.5 or 5 mg/kg/day) on the short-term memory in AD mice was tested in a Y-maze test. After 10 months of administration, quetiapine prevented the decrease of conditioned anxiety and cerebral BDNF in AD mice. In addition, quetiapine also prevented memory impairment in the Y-maze test in AD mice. These findings suggest that the therapeutic mechanism of quetiapine on anxiety in AD may be associated with its beneficial effect on memory and its neuroprotective effect on cerebral BDNF expression.

Our previous study has shown the preventive effects of quetiapine, an atypical antipsychotic drug, on memory impairment and brain pathological changes in a mouse model of Alzheimer's disease (AD). The aim of the present study was to evaluate the therapeutic effects of quetiapine on memory deficit and neuropathology in an amyloid precursor protein (APP)/presenilin-1 (PS1) double transgenic mouse model of AD. The APP/PS1 mice started to have detectable brain β-amyloid (Aβ) at 3 months of age. Non-transgenic and transgenic mice were treated with quetiapine (0, 2.5, or 5 mg/(kg day)) in drinking water from the age of 4 months. After 8 months of continuous quetiapine administration, memory deficit was reversed and brain Aβ plaque pathology was attenuated in the AD mice. Quetiapine also decreased the soluble Aβ peptide levels in brain and cerebrospinal fluid (CSF), and attenuated the decreased synaptic protein levels in the AD mice. Furthermore, quetiapine normalized the abnormal activity of glycogen synthase kinase-3β (GSK-3β), an AD-involved kinase, in the AD mice. These results suggest that quetiapine can treat and alleviate the neuropathology in an APP/PS1 transgenic mouse model of AD, and indicate that quetiapine may have therapeutic effects in the treatment of AD.

Serum levels of β-amyloid (Aβ) peptides may represent an early biomarker in the diagnosis of Alzheimer's disease (AD). In the present study, we investigated the temporal kinetic changes in the levels of serum Aβ 1-42 and 40 in an amyloid precursor protein (APP)/presenilin (PS)1 double transgenic mouse model of AD. Serum Aβ peptide levels in 2-, 3-, 6-, 9- and 18-month old, and liver Aβ 1-40 level in 6-month old mice were measured using enzyme-linked immunosorbent assay (ELISA) kits. Results revealed that serum Aβ levels peaked in 3-month old transgenic mice, and the Aβ level in non-transgenic and transgenic mice is comparable in liver. Compared to the 6-month old transgenic mice, Congo red staining showed that the 3-month old transgenic mice had minimum brain Aβ plaques, corresponding to the early stage of Alzheimer-like plaque pathology, and confocal microscope images showed that the deposition of Aβ in their cerebral vessels was minimal. Furthermore, results of the water maze test, showed that memory was normal for the 3- month old transgenic mice when compared to age-matched non-transgenic mice. These results suggest that serum Aβ peptide levels may be peaked during the early stage of AD. Monitoring serum Aβ peptide levels in the potential AD population may provide an early diagnosis of AD prior to the appearance of clinical symptoms.

There is a paucity of research on spontaneous recovery (SR) from substance abuse in general, and specific to Aboriginal peoples. There is also limited understanding of the healing process associated with SR. In this study, SR was examined among a group of Aboriginal peoples in Canada. Employing a decolonizing methodology, thematic analysis of traditional talking circle narratives identified an association between a traumatic life event and an ‘awakening.’ This ‘awakening’ was embedded in primary (i.e., consider impact on personal well-being) and secondary (i.e., implement alternative coping mechanism) cognitive appraisal processes and intrinsic and extrinsic motivation rooted in increased traditional Aboriginal cultural awareness and understanding. This contributed to both abstinence (i.e., recovery) and sustained well-being (i.e., continued abstinence). Three key interrelated ‘themes’ specific to the role of culture in SR and recovery maintenance were identified: Aboriginal identity, cultural practices, and traditional values. These findings, combined with the limited literature, were developed into a prospective model of SR from substance abuse in Aboriginal peoples. This model highlights the potential need for substance abuse treatment and intervention policy to consider culture as a determinant of health and well-being.

Previous studies have suggested that quetiapine, a new atypical antipsychotic drug, may have beneficial effects on cognitive impairment and be a neuroprotectant in treating neurodegenerative diseases. In the present study, we investigated the effects of quetiapine on memory impairment and its possible neuroprotective effects in an amyloid precursor protein (APP)/presenilin1 (PS1) double transgenic mouse model of Alzheimer's disease (AD). Non-transgenic and transgenic mice were treated with quetiapine (0, 2.5, or 5 mg/kg/day) in drinking water from the age of 2 months. After continuous treatment with quetiapine for 4 months, mice were tested for memory on a water maze task. After the behavioral test, mice were sacrificed for Western blot and biochemical measurements at the age of 6 months. The chronic administration of quetiapine prevented memory impairment in the transgenic mice. Furthermore, quetiapine up-regulated cerebral Bcl-2 protein, and attenuated cerebral nitrotyrosine, a protein marker of oxidative stress in the transgenic mice. These findings suggest that quetiapine can alleviate cognitive impairment in an APP/PS1 double transgenic mouse model of AD, and further indicate that quetiapine may have preventive and neuroprotective effects in the treatment of AD.

Previous studies have suggested that quetiapine, an atypical antipsychotic drug, may have beneficial effects on cognitive impairment, and be a neuroprotectant in treating neurodegenerative diseases. In the present study, we investigated the effects of quetiapine on memory impairment and pathological changes in an amyloid precursor protein (APP)/presenilin-1 (PS-1) double transgenic mouse model of Alzheimer's disease (AD). Non-transgenic and transgenic mice were treated with quetiapine (0, 2.5, or 5mg/(kg day)) for 1, 4, and 7 months in drinking water from the age of 2 months. After 4 and 7 months of continuous quetiapine administration, memory impairment was prevented, and the number of beta-amyloid (Abeta) plaques decreased in the cortex and hippocampus of the transgenic mice. Quetiapine also decreased brain Abeta peptides, beta-secretase activity and expression, and the level of C99 (an APP C-terminal fragment following cleavage by beta-secretase) in the transgenic mice. Furthermore, quetiapine attenuated anxiety-like behavior, up-regulated cerebral Bcl-2 protein, and decreased cerebral nitrotyrosine in the transgenic mice. These findings suggest that quetiapine can alleviate cognitive impairment and pathological changes in an APP/PS1 double transgenic mouse model of AD, and further indicate that quetiapine may have preventive effects in the treatment of AD.