Dear colleagues,
It is my great pleasure to introduce to you the third issue of 2019 featuring original research on Alzheimer’s disease and cognition.
In a commentary, Kranz and Kasper comment on the suitability of medical analogies, from hypertension to broken leg. The authors discuss the view on psychiatric disorders and the use of a metaphor to illustrate those.
Müller and colleagues review the therapeutic efficacy of the Ginkgo special extract Egb 761® within the framework of the mitochondrial cascade hypothesis of Alzheimer’s disease. They discuss the most relevant publications on the effects of Egb 761® on cognition and synaptic deficits. The Ginkgo extract improves mitochondrial dysfunction and cognitive impairment over the whole spectrum of age-associated cognitive disorders in animal models and in vitro experiments. In clinical settings, it improves cognition of the whole range, from aging to Alzheimer’s or even vascular dementia. The authors conclude that the Gingko extract therefore can serve as an important pharmacological argument for the mitochondrial cascade hypothesis of dementia.
Costa et al., assessed the plasma lipids metabolism in mild cognitive impairment (MCI) and Alzheimer’s disease (AD) patients. The study failed to fix the ten phospholipids as a panel to predict Alzheimer’s disease, however the authors suggest that lipid metabolites in plasma might indirectly indicate changes in neuronal membrane, which could possibly outline the transition between healthy and diseased brains.
Hirjak and associates aimed to assess the relevance of hippocampal subfield integrity and clock drawing test (CDT) performance for the diagnosis of Alzheimer’s disease (AD) and mild cognitive impairment (MCI). The authors found that impaired CDT performance in AD was associated with widespread atrophy of the cornu ammonis, presubiculum and subiculum. MCI subjects showed CDT-related alterations of the CA4-dentate gyrus and subiculum. The findings support the theory of the involvement of different hippocampal subfields in impaired CDT performance in AD and MCI patients.
Teixeira and colleagues evaluated the effects of exercise on cognitive function in hypertensive and diabetic patients using the mental test and training system. Participants with systemic arterial hypertension and diabetes mellitus demonstrated significantly improved attention and concentration, but not reaction time, following supervised exercise during 12 weeks. The results indicate that structured physical training promotes several aspects of cognitive functions.
Elkana et al., showed that cognitive function is largely intact in methadone maintenance treatment (MTT) patients. Despite heterogeneity in MTT duration, abuse duration, substance use and psychiatric comorbidity, all subjects performed within ±1 standard deviation of average for age and education in most cognitive domains. The findings may lead to reduced bias regarding cognitive function of MMT patients.
De Vries and associates analysed cognitive control networks in OCD: A resting-state connectivity study in unmedicated patients with obsessive-compulsive disorder and their unaffected relatives. Increased within- and between- network connectivity in siblings, but not in patients was found, which could indicate a mechanism of increased cognitive control that may act as protective mechanism. However, none of the observed network alterations can be considered an endophenotype for OCD since differences were present in either patients or siblings, but not in both groups.
In a brief report, Segal-Gavish and colleagues report that voluntary exercise improves cognitive deficits in female dominant-negative DISC1 transgenic mouse model of neuropsychiatric disorders. Voluntary exercise improved performance in the novel object recognition test, restored the impairment in spatial memory in the Y maze and reversed the deficit in social recognition memory in DN-DISC1 female. DN-DISC1 males did not exhibit behavioural deficits at baseline. Tissue analysis also revealed that exercise induced a significant increase in hippocampal expression of doublecortin (DCX), brain-derived neurotrophic factor (BDNF) and cannabinoid receptor type 1 (CB1R) only in DN-DISC1 females.
Yours sincerely,