Recent accounts of major depression have tended to focus on dysfunction of frontothalamic-striatal reentrant circuits as a possible source of the disorder. Evidence of frontostriatal involvement in unipolar major depression from lesion and neuropsychological studies, and functional and structural imaging studies is examined. The high incidence of depressive symptomatology following left frontal and basal ganglia lesions implicate these as possible sites of dysfunction. Neuropsychological evidence indicates similar deficits in patients with major depression, perhaps with dorsolateral prefrontal deficits most prominent. Structural imaging studies report frontal and basal ganglia (BG) abnormalities particularly in cases of late-age onset depression. Resting state functional imaging studies show deficits in dorsolateral, anterior cingulate (medial frontal), and BG structures. Activation imaging studies show less consistent evidence of dorsolateral deficit, while anterior cingulate deficit is more consistently demonstrated. Variability in findings across studies may reflect differences between subtypes of depression and differences in methodology. Possible involvement of the BG in the psychomotor retardation of depression is examined. It is concluded that, while there is evidence of frontostriatal deficit in major depression, the exact nature of such deficits is uncertain. Issues such as component vs. system dysfunction need to be addressed.
"ence Increased left - intra - hemispheric coherence ( F3 – P3 ) was specific to the MBCT group , compared to right - hemi - spheric coherence ( F4 – P4 ) in the WL . These findings suggest MBCT enhanced fronto - parietal connectivity within the left - hemisphere , where left frontal hypoactivity is a consistent finding in MDD ( Ohta et al . 2008 ; Rogers et al . 1998 ( review ) ; Bajulaiye and Alexopoulos 1994 ) . Moreover , enhanced long - range fronto - parietal coherence was exclusive to the α - band , whereby increased α - coher - ence has been linked to fluid complex higher - order functions , such as central executive control ( Sauseng et al . 2005 : also specific to the fronto - parietal netw"
[Show abstract][Hide abstract] ABSTRACT: To illuminate candidate neural working mech-anisms of Mindfulness-Based Cognitive Therapy (MBCT) in the treatment of recurrent depressive disorder, parallel to the potential interplays between modulations in electro-cortical dynamics and depressive symptom severity and self-compassionate experience. Linear and nonlinear α and γ EEG oscillatory dynamics were examined concomitant to an affective Go/NoGo paradigm, pre-to-post MBCT or natural wait-list, in 51 recurrent depressive patients. Spe-cific EEG variables investigated were; (1) induced event-related (de-) synchronisation (ERD/ERS), (2) evoked power, and (3) inter-/intra-hemispheric coherence. Sec-ondary clinical measures included depressive severity and experiences of self-compassion. MBCT significantly downregulated α and γ power, reflecting increased cortical excitability. Enhanced α-desynchronisation/ERD was observed for negative material opposed to attenuated α-ERD towards positively valenced stimuli, suggesting acti-vation of neural networks usually hypoactive in depression, related to positive emotion regulation. MBCT-related increase in left-intra-hemispheric α-coherence of the fron-to-parietal circuit aligned with these synchronisation dynamics. Ameliorated depressive severity and increased self-compassionate experience pre-to-post MBCT corre-lated with α-ERD change. The multi-dimensional neural mechanisms of MBCT pertain to task-specific linear and non-linear neural synchronisation and connectivity network dynamics. We propose MBCT-related modulations in dif-fering cortical oscillatory bands have discrete excitatory (enacting positive emotionality) and inhibitory (disengag-ing from negative material) effects, where mediation in the α and γ bands relates to the former. Keywords Major Depressive Disorder (MDD) · Mindfulness-Based Cognitive Therapy (MBCT) · ERD/ERS · Oscillatory EEG · α-Band coherence · γ-Band · EEG power Introduction
"It should be borne in mind that serotonin nerve endings are present in large numbers in both analyzed brain structures. Some authors demonstrated that striatal dopamine play an important role in the pathophysiology of depression by modulating emotional and motor symptoms (Byrum et al. 1999; Newberg et al. 2007; Rogers et al. 1998). Additionally, Amsterdam et al. (2012) suggested that greater striatal dopamine transporter density may represent a putative biomarker of depression. "
[Show abstract][Hide abstract] ABSTRACT: Oxidative stress is a major contributing factor in a range of brain pathologies and in the etiology of depression. 1-Methyl-1,2,3,4-tetrahydroisoquinoline (1MeTIQ) is an endogenous substance which is present in the mammalian brain and exhibits neuroprotective, and monoamine oxidase (MAO)-inhibiting properties. In the present study, in order to investigate the potential role of 1MeTIQ as an antidepressant, we tested antidepressant-like effects of 1MeTIQ in comparison with desipramine (a classic antidepressant) in the forced swimming test (FST), and using HPLC methodology, we measured the concentrations of monoamines (dopamine, noradrenaline, serotonin) and the rate of their metabolism. 1MeTIQ given alone as well as in combination with desipramine produced an antidepressant-like effect and decreased the immobility time in the FST. Neurochemical data have shown that 1MeTIQ like desipramine, activated the noradrenergic system. However, the mechanism of action of 1MeTIQ is broader than the actions of desipramine, and 1MeTIQ inhibits the MAO-dependent oxidation of dopamine and serotonin in all investigated structures. We can conclude that 1MeTIQ exhibits antidepressant-like activity in the FST in the rat. The mechanism of its antidepressant action differs from desipramine and seems to be mostly associated with the inhibition of the catabolism of monoamines and their increased concentrations in the brain. 1MeTIQ seems to be very beneficial from the clinical point of view as a reversible MAO inhibitor with a significant antidepressant effects.
Neurotoxicity Research 09/2013; 25(4). DOI:10.1007/s12640-013-9425-0 · 3.54 Impact Factor
"This finding extends previous reports of cognitive differences between late-onset and early-onset MDD patients (Herrmann et al. 2007). These pronounced deficits might be related to progressive abnormalities in cortico-striatal-pallidal-thalamic circuits that have been identified in MDD (Rogers et al. 1998 ; Marchand & Yurgelun-Todd, 2010 ; Bora et al. 2012 b) as well as vascular changes in white matter (Herrmann et al. 2008). Verbal memory problems might be related to a risk of future neurodegenerative disorders in some of these patients (Yeh et al. 2011 ; Vilalta-Franch et al. 2012). "
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