SLEEP-DISORDERED BREATHING, A disorder characterized by recurrent arousals from sleep and intermittent hypoxemia, is common among older adults and affects up to 60% of elderly populations. A number of adverse health outcomes including hypertension, cardiovascular disease, and diabetes have been associated with sleep-disordered breathing. Cognitive impairment also has been linked to sleep-disordered breathing, but the majority of studies have been crosssectional or have relied on nonobjective measures of sleep-disordered breathing, thus limiting the ability to draw conclusions on the directionality of the association. It remains unclear whether sleep-disordered breathing precedes cognitive impairment in communitydwelling elderly individuals. Given the high prevalence and significant morbidity associated with both sleep-disordered breathing and cognitive impairment in older populations, establishing whether a prospective association exists between sleep-disordered breathing and cognition is important. This is especially important because ef-

Sleep disordered breathing, hypoxia, and risk of mild cognitive impairment and dementia in older women

Experimental models of epilepsy are useful to identify potential mechanisms of epileptogenesis, seizure genesis, comorbidities, and treatment efficacy. The kainic acid (KA) model is one of the most commonly used. Several modes of administration of KA exist, each producing different effects in a strain-, species-, gender-, and age-dependent manner. In this review, we discuss the advantages and limitations of the various forms of KA administration (systemic, intrahippocampal, and intranasal), as well as the histologic, electrophysiological, and behavioral outcomes in different strains and species. We attempt a personal perspective and discuss areas where work is needed. The diversity of KA models and their outcomes offers researchers a rich palette of phenotypes, which may be relevant to specific traits found in patients with temporal lobe epilepsy.

/pdf/the-kainic-acid-models-of-temporal-lobe-epilepsy-4jz6dhkirx.pdf

The Kainic acid models of Temporal Lobe Epilepsy

Alzheimer's disease (AD) has become a severe medical challenge. Advances in technologies produced high-dimensional data of different modalities including functional magnetic resonance imaging (fMRI) and single nucleotide polymorphism (SNP). Understanding the complex association patterns among these heterogeneous and complementary data is of benefit to the diagnosis and prevention of AD. In this paper, we apply the appropriate correlation analysis method to detect the relationships between brain regions and genes, and propose “brain region-gene pairs” as the multimodal features of the sample. In addition, we put forward a novel data analysis method from technology aspect, cluster evolutionary random forest (CERF), which is suitable for “brain region-gene pairs”. The idea of clustering evolution is introduced to improve the generalization performance of random forest which is constructed by randomly selecting samples and sample features. Through hierarchical clustering of decision trees in random forest, the decision trees with higher similarity are clustered into one class, and the decision trees with the best performance are retained to enhance the diversity between decision trees. Furthermore, based on CERF, we integrate feature construction, feature selection and sample classification to find the optimal combination of different methods, and design a comprehensive diagnostic framework for AD. The framework is validated by the samples with both fMRI and SNP data from ADNI. The results show that we can effectively identify AD patients and discover some brain regions and genes associated with AD significantly based on this framework. These findings are conducive to the clinical treatment and prevention of AD.

Multimodal Data Analysis of Alzheimer's Disease Based on Clustering Evolutionary Random Forest

The role of adenosine in epilepsy

Novel therapeutic approaches for disease-modification of epileptogenesis for curing epilepsy

Rapid changes in expression of class I and IV histone deacetylases during epileptogenesis in mouse models of temporal lobe epilepsy

Epigenetic mechanisms like altered histone acetylation may have a crucial role in epileptogenesis. In two mouse models of temporal lobe epilepsy, we investigated changes in the expression of class II histone deacetylases (HDAC), a group of signal transducers that shuttle between nucleus and cytoplasm. Intrahippocampal injection of kainic acid (KA) induced a status epilepticus, development of spontaneous seizures (after 3 days), and finally chronic epilepsy and granule cell dispersion. Expression of class II HDAC mRNAs was investigated at different time intervals after KA injection in the granule cell layers and in sectors CA1 and CA3 contralateral to the site of KA injection lacking neurodegeneration. Increased expression of HDAC5 and 9 mRNAs coincided with pronounced granule cell dispersion in the KA‐injected hippocampus at late intervals (14–28 days after KA) and equally affected both HDAC9 splice variants. In contrast, in the pilocarpine model (showing no granule cell dispersion), we observed decreases in the expression of HDAC5 and 9 at the same time intervals. Beyond this, striking similarities between both temporal lobe epilepsy models such as fast decreases in HDAC7 and 10 mRNAs during the acute status epilepticus were observed, notably also in the contralateral hippocampus not affected by neurodegeneration. The particular patterns of HDAC mRNA expression suggest a role in epileptogenesis and granule cell dispersion. Reduced expression of HDACs may result in increased expression of pro‐ and anticonvulsive proteins. On the other hand, export of HDACs from the nucleus into the cytoplasm could allow for deacetylation of cytoplasmatic proteins involved in axonal and dendritic remodeling, like granule cell dispersion.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/jnc.13440

Expression of class II histone deacetylases in two mouse models of temporal lobe epilepsy.

Corticothalamic network dysfunction and Alzheimer’s disease

Sleep disruptions promote increases of amyloid β (Aβ) and tau in the brain and increase Alzheimer’s disease (AD) risk, but the precise mechanisms that give rise to sleep disturbances have yet to be...

Restoring activity in the thalamic reticular nucleus improves sleep architecture and reduces Aβ accumulation in mice.

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Rapid changes in expression of class I and IV histone deacetylases during epileptogenesis in mouse models of temporal lobe epilepsy

Expression of class II histone deacetylases in two mouse models of temporal lobe epilepsy.

Corticothalamic network dysfunction and Alzheimer’s disease

Restoring activity in the thalamic reticular nucleus improves sleep architecture and reduces Aβ accumulation in mice.