The Influence of Aging on Poststroke Depression Using a Rat Model via Middle Cerebral Artery Occlusion.

The influence of aging on poststroke depression using a rat model via middle cerebral artery occlusion.

Cogn Affect Behav Neurosci. 2013 Jun 13;
Boyko M, Kutz R, Gruenbaum BF, Cohen H, Kozlovsky N, Gruenbaum SE, Shapira Y, Zlotnik A

Poststroke depression (PSD) is the most frequent psychological sequela following stroke. While previous studies describe the impact of age on brain infarct volume, brain edema, and blood-brain barrier (BBB) breakdown following ischemia, the role of age on PSD has yet to be described. Here, we examine the influence of age on PSD progression in a rat model of PSD by middle cerebral artery occlusion (MCAO). One hundred forty-three rats were divided into three groups. 48 rats 20 weeks of age underwent a sham procedure, 51 rats 20 weeks of age had MCAO, and 44 rats 22-26 months of age had MCAO. Groups were further divided into two subgroups. The first subgroup was used to measure infarct lesion volume, brain edema, and BBB breakdown at 24 h. In the second subgroup at 3 weeks after MCAO, rats were subjected to a sucrose preference test, two-way shuttle avoidance task, forced swimming test, and a brain-derived neurotrophic factor (BDNF) protein level measurement. Total and striatal infarct volume, brain edema, and BBB breakdown in the striatum were increased in older rats, as compared with younger rats. While both old and young rats exhibited depressive-like behaviors on each of the behavioral tests and lower BDNF levels post-MCAO, as compared with control rats, there were no differences between old and young rats. Although older rats suffered from larger infarct volumes, increased brain edema and more BBB disruption following MCAO, the lack of behavioral differences between young and old rats suggests that there was no effect of rat age on the incidence of PSD. HubMed – depression


[Rapid-progressive decrease of cognitive and physical functions in a B-cell non-Hodgkin’s lymphoma patient treated with rituximab/bendamustine].

Dtsch Med Wochenschr. 2013 Jun; 138(25-26): 1355-9
Küllmer A, Herrmann G, Riecken B

History: A 71-year-old man with Richter’s syndrome (transformation of chronic lymphocytic leukemia [CLL] to diffuse large B-cell lymphoma) was admitted to our hospital to get his second cycle of rituximab/bendamustin treatment. He had been diagnosed with Richter’s syndrome three months earlier: a bulky tumor was seen on the backside of the stomach in a routine gastroscopy. Taking a biopsy had resulted in a major bleeding impossible to stop endoscopically. An emergency surgical multi-visceral resection was performed. The first cycle of chemotherapy was administered about 4 weeks prior to the present appointment.Investigations: In the physical examination the patient showed a bad orientation and confusion together with a skinny habitus. The initially performed lab tests and a CT-Scan of the brain did not show a significant finding. A mini-mental-state-examination (MMSE) showed moderate cognitive impairment. In a psychiatric consultation the patient was diagnosed with reactive depression and a corresponding medication was given. After the second cycle of chemotherapy the patient’s state of mind decreased markedly within days.Diagnosis, treatment and further course: The further diagnostic investigation (MRI of the brain, lumbar puncture) brought the diagnosis of progressive multifocal leukoencephalopathy. The administration of chemotherapy was stopped then. Three weeks after the diagnosis the patient died in the hospice.Conclusion: If a patient develops neurological or psychiatric symptoms during therapy with rituximab clinicians should be aware of the potential diagnosis of PML and initiate further investigations. HubMed – depression


Coenzyme Q10 Depletion in Medical and Neuropsychiatric Disorders: Potential Repercussions and Therapeutic Implications.

Mol Neurobiol. 2013 Jun 13;
Morris G, Anderson G, Berk M, Maes M

Coenzyme Q10 (CoQ10) is an antioxidant, a membrane stabilizer, and a vital cofactor in the mitochondrial electron transport chain, enabling the generation of adenosine triphosphate. It additionally regulates gene expression and apoptosis; is an essential cofactor of uncoupling proteins; and has anti-inflammatory, redox modulatory, and neuroprotective effects. This paper reviews the known physiological role of CoQ10 in cellular metabolism, cell death, differentiation and gene regulation, and examines the potential repercussions of CoQ10 depletion including its role in illnesses such as Parkinson’s disease, depression, myalgic encephalomyelitis/chronic fatigue syndrome, and fibromyalgia. CoQ10 depletion may play a role in the pathophysiology of these disorders by modulating cellular processes including hydrogen peroxide formation, gene regulation, cytoprotection, bioenegetic performance, and regulation of cellular metabolism. CoQ10 treatment improves quality of life in patients with Parkinson’s disease and may play a role in delaying the progression of that disorder. Administration of CoQ10 has antidepressive effects. CoQ10 treatment significantly reduces fatigue and improves ergonomic performance during exercise and thus may have potential in alleviating the exercise intolerance and exhaustion displayed by people with myalgic encepholamyletis/chronic fatigue syndrome. Administration of CoQ10 improves hyperalgesia and quality of life in patients with fibromyalgia. The evidence base for the effectiveness of treatment with CoQ10 may be explained via its ability to ameliorate oxidative stress and protect mitochondria. HubMed – depression



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