- Delirium and topographical disorientation associated with glioblastoma multiforme tumour progression into the isthmus of the cingulate gyrus. [Journal Article]
- BCBMJ Case Rep 2018 Aug 17; 2018
- Since there is no cure for glioblastoma multiforme (GBM), the goal of treatment becomes prolonging the survival through cytoreduction while minimising neurological deficits. In this case report, lase...
Since there is no cure for glioblastoma multiforme (GBM), the goal of treatment becomes prolonging the survival through cytoreduction while minimising neurological deficits. In this case report, laser interstitial thermal therapy (LITT) was used once the tumour progressed into the isthmus of the cingulate gyrus. One year after temporal lobectomy, disorders of memory, emotion, personality and navigation, likely related to limbic system involvement along with hallucinations and fluctuating cognition occurred as the tumour progressed. After ablation of the posterior cingulum, worsening of topographical disorientation was observed.Per literature review, delirium has been noted in patients with strokes involving the right-sided temporo-parieto-occipital junction, and topographical disorientation has been associated with lesions of the right posterior cingulum. Alternative causes of these deficits were ruled out, leaving structural changes as the primary explanation. This is the first report of the neurological deficits associated with tumour progression and vasogenic oedema in this region.
- Role of DHEA and cortisol in prefrontal-amygdalar development and working memory. [Journal Article]
- PPsychoneuroendocrinology 2018 Aug 07; 98:86-94
- There is accumulating evidence that both dehydroepiandrosterone (DHEA) and cortisol play an important role in regulating physical maturation and brain development. High DHEA levels tend to be associa...
There is accumulating evidence that both dehydroepiandrosterone (DHEA) and cortisol play an important role in regulating physical maturation and brain development. High DHEA levels tend to be associated with neuroprotective and indirect anabolic effects, while high cortisol levels tend to be associated with catabolic and neurotoxic properties. Previous literature has linked the ratio between DHEA and cortisol levels (DC ratio) to disorders of attention, emotional regulation and conduct, but little is known as to the relationship between this ratio and brain development. Due to the extensive links between the amygdala and the cortex as well as the known amygdalar involvement in emotional regulation, we examined associations between DC ratio, structural covariance of the amygdala with whole-brain cortical thickness, and validated report-based measures of attention, working memory, internalizing and externalizing symptoms, in a longitudinal sample of typically developing children and adolescents 6-22 years of age. We found that DC ratio predicted covariance between amygdalar volume and the medial anterior cingulate cortex, particularly in the right hemisphere. DC ratio had a significant indirect effect on working memory through its impact on prefrontal-amygdalar covariance, with higher DC ratios associated with a prefrontal-amygdalar covariance pattern predictive of higher scores on a measure of working memory. Taken together, these findings support the notion, as suggested by animal and in vitro studies, that there are opposing effects of DHEA and cortisol on brain development in humans, and that these effects may especially target prefrontal-amygdalar development and working memory, in a lateralized fashion.
- Gamma oscillations in cognitive disorders. [Review]
- COCurr Opin Neurobiol 2018 Aug 16; 52:182-187
- Gamma oscillations (∼25-100 Hz) are believed to play a role in cognition. Accordingly, aberrant gamma oscillations have been observed in several cognitive disorders, including Alzheimer's disease and...
Gamma oscillations (∼25-100 Hz) are believed to play a role in cognition. Accordingly, aberrant gamma oscillations have been observed in several cognitive disorders, including Alzheimer's disease and Fragile X syndrome. Here, we review how recent results showing abnormal gamma rhythms in Alzheimer's disease and Fragile X syndrome help reveal links between cellular disturbances and cognitive impairments. We also discuss how gamma results from rodent models of Alzheimer's disease and Fragile X syndrome may provide insights about unique functions of distinct slow (∼25-50 Hz) and fast gamma (∼55-100 Hz) subtypes. Finally, we consider studies employing brain stimulation paradigms in Alzheimer's disease and discuss how such studies may reveal causal relationships between gamma impairments and memory disturbances.
- Cerebrovascular disease influences functional and structural network connectivity in patients with amnestic mild cognitive impairment and Alzheimer's disease. [Journal Article]
- ARAlzheimers Res Ther 2018 Aug 18; 10(1):82
- CONCLUSIONS: We demonstrate differential functional and structural network changes between aMCI and AD patients with and without CeVD through diverging and deleterious network-based degeneration underlying domain-specific cognitive impairment.
- Degradation of Caytaxin Causes Learning and Memory Deficits via Activation of DAPK1 in Aging. [Journal Article]
- MNMol Neurobiol 2018 Aug 17
- Loss of memory is an inevitable clinic sign in aging, but its underlying mechanisms remain unclear. Here we show that death-associated protein kinase (DAPK1) is involved in the decays of learning and...
Loss of memory is an inevitable clinic sign in aging, but its underlying mechanisms remain unclear. Here we show that death-associated protein kinase (DAPK1) is involved in the decays of learning and memory in aging via degradation of Caytaxin, a brain-specific member of BNIP-2. DAPK1 becomes activated in the hippocampus of mice during aging. Activation of DAPK1 is closely associated with degradation of Caytaxin protein. Silencing Caytaxin by the expression of small interfering RNA (siRNA) that targets specifically to Caytaxin in the hippocampus of adult mice impairs the learning and memory. Genetic inactivation of DAPK1 by deletion of DAPK1 kinase domain prevents the degradation of Caytaxin and protects against learning and memory declines. Thus, activation of DAPK1 impairs learning and memory by degrading Caytaxin during aging.
- Learning Without Trying: The Clinical Relevance of Statistical Learning. [Journal Article]
- LSLang Speech Hear Serv Sch 2018 Aug 14; 49(3S):710-722
- CONCLUSIONS: The statistical learning literature offers principles for learning that can improve clinical outcomes for children with language impairment. There is potential for further applications of this basic research that is yet unexplored.
- Altered ErbB4 splicing and cortical parvalbumin interneuron dysfunction in schizophrenia and mood disorders. [Journal Article]
- NNeuropsychopharmacology 2018 Aug 02
- Working memory requires the activity of parvalbumin (PV) interneurons in the dorsolateral prefrontal cortex (DLPFC). Impaired working memory and lower PV expression in the DLPFC are reported in schiz...
Working memory requires the activity of parvalbumin (PV) interneurons in the dorsolateral prefrontal cortex (DLPFC). Impaired working memory and lower PV expression in the DLPFC are reported in schizophrenia and to a lesser degree in mood disorders. We previously proposed that activity-dependent PV expression is lower in schizophrenia due to a shift in the splicing of erb-b2 receptor tyrosine kinase 4 (ErbB4) transcripts from major to inactive minor variants that reduces excitatory drive to PV interneurons. Here, we tested the hypothesis that the degree of major-to-minor shift in ErbB4 splicing predicts the level of PV expression across schizophrenia and mood disorders. Levels of ErbB4 splice variants and PV mRNA were quantified by PCR in the DLPFC from 40 matched tetrads (N = 160 subjects) of schizophrenia, bipolar disorder (BD), major depressive disorder (MDD), and unaffected comparison subjects. Relative to unaffected comparison subjects, the magnitude of increases in minor variant levels and decreases in major variant levels was greatest in schizophrenia, intermediate in BD, and least in MDD. The same rank order was present for the magnitude of increases in the composite splicing score, which reflects the degree of major-to-minor shift across all ErbB4 splice loci, and for the magnitude of deficient PV expression. Finally, the composite splicing score negatively predicted PV expression across all subject groups. Together, these findings demonstrate a shared relationship between ErbB4 splicing and PV expression and suggest that scaling of the major-to-minor shift in ErbB4 splicing may influence the severity of deficient PV interneuron activity across diagnoses.
- Hypertension-induced cognitive impairment: insights from prolonged angiotensin II infusion in mice. [Journal Article]
- HRHypertens Res 2018 Aug 17
- The causal relation between hypertension and cerebral small vessel disease (cSVD) remains elusive, and appropriate animal models are scarce. We aimed to assess the relevance of prolonged angiotensin ...
The causal relation between hypertension and cerebral small vessel disease (cSVD) remains elusive, and appropriate animal models are scarce. We aimed to assess the relevance of prolonged angiotensin II-induced hypertension in mice for the study of cSVD.Adult male C57BL/6 mice were continuously infused for 3 months with Angiotensin II (Ang II; 2 µg/kg/min, sc) or saline (control) via osmotic minipumps. Blood pressure, neurological function, locomotor activity, and working memory (Y-maze alternation task) were assessed throughout the study. Short-term memory performance (object location task) was measured after 3 months of infusion. Blood-brain barrier (BBB) function was assessed by the presence of IgG leakage and quantified in each brain area of interest. Microglial activation and myelin loss were studied in the areas of leakage.Systolic blood pressure increased and remained elevated over the 3 months of Ang II infusion, while neurological scores and locomotor activity did not change. Working memory performance was also not changed, yet short-term memory performance was impaired in Ang II-treated mice compared to controls. While BBB leakages were present in both groups, mainly in the neocortex, hippocampus, and cerebral nuclei, Ang II-treated mice showed greater leakage than control mice, along with greater microglial density and soma size. Myelin loss was observed for the largest leaks.Prolonged Ang II-induced hypertension is associated with large BBB leaks, microglial activation, myelin loss, and memory dysfunction in the absence of stroke.
- Loss of thin spines and small synapses contributes to defective hippocampal function in aged mice. [Journal Article]
- NANeurobiol Aging 2018 Jul 24; 71:91-104
- Aging is a normal physiological process associated with impairments in cognitive function, including learning and memory. Here, the underlying synaptic mechanisms by which aging leads to the decline ...
Aging is a normal physiological process associated with impairments in cognitive function, including learning and memory. Here, the underlying synaptic mechanisms by which aging leads to the decline of spatial learning and memory function were investigated in 25-month-old aged mice versus 2-month-old young mice. Deficits of spatial learning and memory, as well as selective loss of thin spines, but not mushroom-type spines on apical dendrites of CA1 pyramidal cells were found in aged mice. Specifically, loss of thin spines in aged mice with memory deficits was primarily found on dendritic segments located in the Schaffer pathway, and the density of thin spines significantly correlated with spatial memory performance. The loss of thin spines was evidenced by a decrease in small synapses that express diminutive amounts of postsynaptic density protein-95 and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit GluR1. Furthermore, mushroom-type spines and GluR1-expressed large synapses were not affected in aged mice with impaired memory. Taken together, these data suggest that the selective loss of those highly plastic thin spines with sparse postsynaptic density protein-95 and GluR1 receptors may significantly contribute to cognitive deficits in aged individuals.
New Search Next
- The opioid system in stress-induced memory disorders: From basic mechanisms to clinical implications in posttraumatic stress disorder and Alzheimer's disease. [Review]
- PNProg Neuropsychopharmacol Biol Psychiatry 2018 Aug 14
- Cognitive and emotional impairment are a serious consequence of stress exposure and are core features of neurological and psychiatric conditions that involve memory disorders. Indeed, acute and chron...
Cognitive and emotional impairment are a serious consequence of stress exposure and are core features of neurological and psychiatric conditions that involve memory disorders. Indeed, acute and chronic stress are high-risk factors for the onset of posttraumatic stress disorder (PTSD) and Alzheimer's disease (AD), two devastating brain disorders associated with memory dysfunction. Besides the sympathetic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis, stress response also involves the activation of the opioid system in brain regions associated with stress regulation and memory processing. In this context, it is possible that stress-induced memory disorders may be attributed to alterations in the interaction between the neuroendocrine stress system and the opioid system. In this review, we: (1) describe the effects of acute and chronic stress on memory, and the modulatory role of the opioid system, (2) discuss the contribution of the opioid system to the pathophysiology of PTSD and AD, and (3) present evidence of current and potential therapies that target the opioid receptors to treat PTSD- and AD-associated symptoms.