Abstract:Abstract. Objectives:To investigate the principal psychopathological dimensions of post-stroke depression (PSD) through the assessment of the factorial structure of the Post-Stroke Depression Rating Scale (PSDRS). Methods: We enrolled ninety-eight subjects with PSD, who underwent the PSDRS, MMSE and Barthel Index. Information about demographic, clinical, and neuroanatomical factors was collected.Results: The factor analysis extracted three factors accounting for 63.4% of the total variance, and identified as: … Show more
“…Since the behavior of our aged rodents was more „apathetic“ we hypothesize that the increased HT2B mRNA and protein expression in neurons around the peri-lesional area was due to the interruption of asceding inputs from basal ganglia which normally supply neurons in the frontal cortex with biogenic amines like 5-HT and dopamine. Our hypothesis is supported by animal studies reporting an upregulation of Htr2B mRNA and protein in response to the serotonergic deafferentation to compensate for the loss of serotonin input [ 55 ] and several clinical studies in elderly patients that reported an association between old age and apathy in stroke survivors [ 42 , 56 , 57 ] and normal elderly subjects [ 51 ]. Furthermore, apathy is significantly more represented in late onset depression than in early onset depression [ 58 ].…”
Section: Discussionsupporting
confidence: 69%
“…The pattern of brain distribution suggests that the activation of 5-HT2 receptor subtypes may be implicated in the regulation of mood disorders [ 42 ]. Indeed we found that Htr2B mRNA but not Htr2A mRNA, was robustly increased in the perilesional frontal area of aged rats suggesting that the interruption in the serotoninergic innervation of cortical neurons by stroke may lead to an increased expression of Htr2B mRNA and serotonin receptors in the motor and frontal cortex.…”
Despite the fact that a high proportion of elderly stroke patients develop mood disorders, the mechanisms underlying late-onset neuropsychiatric and neurocognitive symptoms have so far received little attention in the field of neurobiology. In rodents, aged animals display depressive symptoms following stroke, whereas young animals recover fairly well. This finding has prompted us to investigate the expression of serotonin receptors 2A and 2B, which are directly linked to depression, in the brains of aged and young rats following stroke. Although the development of the infarct was more rapid in aged rats in the first 3 days after stroke, by day 14 the cortical infarcts were similar in size in both age groups i.e. 45% of total cortical volume in young rats and 55.7% in aged rats. We also found that the expression of serotonin receptor type B mRNA was markedly increased in the perilesional area of aged rats as compared to the younger counterparts. Furthermore, histologically, HTR2B protein expression in degenerating neurons was closely associated with activated microglia both in aged rats and human subjects. Treatment with fluoxetine attenuated the expression of Htr2B mRNA, stimulated post-stroke neurogenesis in the subventricular zone and was associated with an improved anhedonic behavior and an increased activity in the forced swim test in aged animals. We hypothesize that HTR2B expression in the infarcted territory may render degenerating neurons susceptible to attack by activated microglia and thus aggravate the consequences of stroke.
“…Since the behavior of our aged rodents was more „apathetic“ we hypothesize that the increased HT2B mRNA and protein expression in neurons around the peri-lesional area was due to the interruption of asceding inputs from basal ganglia which normally supply neurons in the frontal cortex with biogenic amines like 5-HT and dopamine. Our hypothesis is supported by animal studies reporting an upregulation of Htr2B mRNA and protein in response to the serotonergic deafferentation to compensate for the loss of serotonin input [ 55 ] and several clinical studies in elderly patients that reported an association between old age and apathy in stroke survivors [ 42 , 56 , 57 ] and normal elderly subjects [ 51 ]. Furthermore, apathy is significantly more represented in late onset depression than in early onset depression [ 58 ].…”
Section: Discussionsupporting
confidence: 69%
“…The pattern of brain distribution suggests that the activation of 5-HT2 receptor subtypes may be implicated in the regulation of mood disorders [ 42 ]. Indeed we found that Htr2B mRNA but not Htr2A mRNA, was robustly increased in the perilesional frontal area of aged rats suggesting that the interruption in the serotoninergic innervation of cortical neurons by stroke may lead to an increased expression of Htr2B mRNA and serotonin receptors in the motor and frontal cortex.…”
Despite the fact that a high proportion of elderly stroke patients develop mood disorders, the mechanisms underlying late-onset neuropsychiatric and neurocognitive symptoms have so far received little attention in the field of neurobiology. In rodents, aged animals display depressive symptoms following stroke, whereas young animals recover fairly well. This finding has prompted us to investigate the expression of serotonin receptors 2A and 2B, which are directly linked to depression, in the brains of aged and young rats following stroke. Although the development of the infarct was more rapid in aged rats in the first 3 days after stroke, by day 14 the cortical infarcts were similar in size in both age groups i.e. 45% of total cortical volume in young rats and 55.7% in aged rats. We also found that the expression of serotonin receptor type B mRNA was markedly increased in the perilesional area of aged rats as compared to the younger counterparts. Furthermore, histologically, HTR2B protein expression in degenerating neurons was closely associated with activated microglia both in aged rats and human subjects. Treatment with fluoxetine attenuated the expression of Htr2B mRNA, stimulated post-stroke neurogenesis in the subventricular zone and was associated with an improved anhedonic behavior and an increased activity in the forced swim test in aged animals. We hypothesize that HTR2B expression in the infarcted territory may render degenerating neurons susceptible to attack by activated microglia and thus aggravate the consequences of stroke.
“…Individuals with PSD exhibit poor rehabilitation outcomes, social isolation, suicidal ideation, and suicide attempts, all of which affect recovery, prolong hospital stays and increase the economic burden compared to non-depressed stroke patients (Cai et al, 2019). With the physiological defect and social dysfunction, PSD also causes cognitive impairments such as attentional decline, impaired memory, and impaired motor function (Quaranta et al, 2012).…”
Shugan Jieyu Capsule (SG), a Chinese herbal medicine mainly composed of Acanthopanax and Hypericum perforatum, has been used to ameliorate cognitive impairments and emotional problems induced by post-stroke depression (PSD), while the altered brain dynamics underlying the ameliorative effects of SG have remained unclear. Our study focused on investigating the potential neurobiological mechanisms of SG in improving the cognitive function of PSD patients via restingstate functional magnetic resonance imaging (fMRI). Fifteen PSD patients (mean ages: 64.13 ± 6.01 years) were instructed to take 0.72 g of SG twice a day for 8 weeks. PSD patients underwent fMRIs, the 24-item Hamilton Depression Scale (HAMD-24) and the Montreal Cognitive Assessment (MoCA) at baseline and the end of intervention, and these assessments were also performed on twenty-one healthy controls (HC) (mean ages: 60.67 ± 6.95 years). Additionally, the dynamic amplitude of low-frequency fluctuations (dALFF) and functional connectivity (dFC) were determined to reveal changes in dynamic functional patterns. We found that taking SG significantly reduced the depressive symptoms assessed by HAMD-24 and improved cognitive functions assessed by MoCA in PSD patients. Furthermore, at baseline, PSD patients showed decreased dALFF in the right precuneus and increased dFC between the right precuneus and left angular gyrus, compared with HC. After intervention, the dALFF and dFC variances of the abnormal patterns were reversed. Additionally, the dALFF variance in the right precuneus was positively correlated with MoCA scores in PSD patients after SG treatment. Collectively, our results indicate that SG may improve the cognitive function of PSD patients through alteration of brain dynamics. Our findings lay a foundation for the exploration of the neurobiological mechanisms of SG in ameliorating symptoms of PSD patients.
“…PSD might be associated with the impairment of other neurological functions such as learning, executive, and motor functions. Most importantly, PSD could negatively influence the functional outcome after stroke rehabilitation and is a risk factor for low quality of life after stroke and a high morbidity [2, 3]. …”
Poststroke depression (PSD) is an important consequence after stroke, with negative impact on stroke outcome. The pathogenesis of PSD is complicated, with some special neurobiological mechanism, which mainly involves neuroanatomical, neuron, and biochemical factors and neurogenesis which interact in complex ways. Abundant studies suggested that large lesions in critical areas such as left frontal lobe and basal ganglia or accumulation of silent cerebral lesions might interrupt the pathways of monoamines or relevant pathways of mood control, thus leading to depression. Activation of immune system after stroke produces more cytokines which increase glutamate excitotoxicity, results in more cell deaths of critical areas and enlargement of infarctions, and, together with hypercortisolism induced by stress or inflammation after stroke which could decrease intracellular serotonin transporters, might be the key biochemical change of PSD. The interaction among cytokines, glucocorticoid, and neurotrophin results in the decrease of hippocampal neurogenesis which has been proved to be important for mood control and pharmaceutical effect of selective serotonin reuptake inhibitors and might be another promising pathway to understand the pathogenesis of PSD. In order to reduce the prevalence of PSD and improve the outcome of stroke, more relevant studies are still required to clarify the pathogenesis of PSD.
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