Mechanism of Disinhibition After Brain Lesions

Starkstein, Sergio E.; Robinson, Robert G.

doi:10.1097/00005053-199702000-00007

Cited by 209 publications

(111 citation statements)

References 27 publications

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“…All of these violations can be regarded as disinhibitory deficits, which are pathologically related to impairments in specific prefrontal cortex regions. For instance, the ventromedial prefrontal cortex is associated with emotion regulation, the anterior cingulate cortex with emotional empathy, and the orbitofrontal cortex with compulsive behavior (Knutson et al, 2015;Mendez, 2010;Starkstein and Robinson, 1997). Related to this, we observed bald patches and in some cases even skin wounds in 75% of the Tau58-2/B male animals, but only in one Wt mouse.…”

Section: Discussionmentioning

confidence: 58%

Impulsivity, decreased social exploration, and executive dysfunction in a mouse model of frontotemporal dementia

Jeugd

Vermaercke

Halliday

et al. 2016

Neurobiology of Learning and Memory

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Frontotemporal lobar degeneration (FTLD) is a neurodegenerative disorder, a major subset of which is characterized by the accumulation of abnormal forms of the protein tau, leading to impairments in motor functions as well as language and behavioral alterations. Tau58-2/B mice express human tau with the P301S mutation found in familial forms of FTLD in neurons. By assessing three age cohorts of Tau58-2/B mice in a comprehensive behavioral test battery, we found that the tauopathy animals showed age-dependent signs of impulsivity, decreased social exploration and executive dysfunction. The deficit in executive function was first limited to decreased spatial working memory, but with aging this was extended to impaired instrumental short-term memory. Tau pathology was prominent in brain regions underlying these behaviors. Thus, Tau-58-2/B mice recapitulate neurological deficits of the behavioral variant of frontotemporal dementia (bvFTD), presenting them as a suitable model to test therapeutic interventions for the amelioration of this variant.2 Keywords: Behavior; executive function; frontotemporal dementia; frontotemporal lobar degeneration; social exploration; tau Highlights• Tau58-2/B mice present with a tau pathology in cortical areas implicated in bvFTD.• Tau58-2/B mice exhibit motor and sensory gating anomalies at an early age.• With aging the mice show decreased sociability but no altered exploration.• The mice further display increased risk-taking behaviors and executive deficits.• First limited to spatial working memory, it later extends to instrumental memory.

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Section: Discussionmentioning

confidence: 58%

Impulsivity, decreased social exploration, and executive dysfunction in a mouse model of frontotemporal dementia

Jeugd

Vermaercke

Halliday

et al. 2016

Neurobiology of Learning and Memory

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“…61 These ventral regions may contribute to the inhibition of prepotent or impulsive responses. [62][63][64] In contrast, limbic targets of ventral frontal cortex, including the dorsal anterior cingulate gyrus and ventral striatum appear to show increased metabolic activity when patients with bipolar disorder are in the manic state. 21 Since the projections from the orbital frontal cortex to the limbic structures are glutamatergic, mania-related hyperactivity may be suggestive of excessive activation of glutamatergic cortico-limbic pathways.…”

Section: Evidence That Mood Stabilizers Attenuate Corticolimbic Glutamentioning

confidence: 99%

Glutamate and GABA systems as targets for novel antidepressant and mood-stabilizing treatments

et al. 2002

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Glutamate and ␥-amino butyric acid (GABA) systems are emerging as targets for development of medications for mood disorders. There is increasing preclinical and clinical evidence that antidepressant drugs directly or indirectly reduce N-methyl-D-aspartate glutamate receptor function. Drugs that reduce glutamatergic activity or glutamate receptor-related signal transduction may also have antimanic effects. Recent studies employing magnetic resonance spectroscopy also suggest that unipolar, but not bipolar, depression is associated with reductions in cortical GABA levels. Antidepressant and mood-stabilizing treatments also appear to raise cortical GABA levels and to ameliorate GABA deficits in patients with mood disorders. The preponderance of available evidence suggests that glutamatergic and GABAergic modulation may be an important property of available antidepressant and mood-stabilizing agents. Future research will be needed to develop and evaluate new agents with specific glutamate and GABA receptor targets in the treatment of mood disorders. Molecular Psychiatry (2002) 7, S71-S80.

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“…Although physical and verbal aggression are the most commonly investigated [8][9][10][11][12][13][14] , there are other serious behavioural outcomes following ABI. These include sexually inappropriate behaviours [15][16][17] , socially inappropriate behaviours 2,6 , absconding 18 , apathy 19,20 , lack of initiation 6 , reduced social skills 21 , disinhibition 22 , irritability 19,23 , and mood disorders 24,25 .…”

Section: Introductionmentioning

confidence: 99%

Family involvement in behaviour management following acquired brain injury (ABI) in community settings: A systematic review

et al. 2015

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Objectives: To examine family involvement in the management of behavioural problems following ABI in the community.Research Design: Systematic literature review.Methods: Six electronic databases relevant to the field of brain injury were searched between 1980-2013. Citation indexes were used, and references from articles hand searched for further literature. Studies that met the broad inclusion criteria were screened for relevance, and articles selected for full-text review independently considered by two reviewers. Those found to be relevant were analysed using PEDro and McMasters critical appraisal tools.Results: Three hundred and three studies were identified after duplicates were removed and 56 were assessed for relevance, yielding 10 studies for review. Although the majority of studies were weak in design, 5 revealed significant findings supportive of family involvement in the management of behavioural problems following ABI, especially where interventions consisted of both educational components and individualised behavioural plans. Findings revealed no significant changes in family burden following behavioural interventions.Conclusions: There is limited research and lack of high evidence studies evaluating family involvement in behaviour management following ABI; therefore no conclusions can be drawn regarding its efficacy. More research is needed, with larger sample sizes and more rigorous design, including proper comparison groups.

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Mechanism of Disinhibition After Brain Lesions

Cited by 209 publications

References 27 publications

Impulsivity, decreased social exploration, and executive dysfunction in a mouse model of frontotemporal dementia

Impulsivity, decreased social exploration, and executive dysfunction in a mouse model of frontotemporal dementia

Glutamate and GABA systems as targets for novel antidepressant and mood-stabilizing treatments

Family involvement in behaviour management following acquired brain injury (ABI) in community settings: A systematic review

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