Recently, circular RNAs (circRNAs) have been revealed to be an important non-coding element of the transcriptome. The brain contains the most abundant and widespread expression of circRNA. There are also indications that the circular transcriptome undergoes dynamic changes as a result of brain ageing.
View Article and Find Full Text PDFNormal aging is associated with impairments in cognitive functions. These alterations are caused by diminutive changes in the biology of synapses, and ineffective neurotransmission, rather than loss of neurons. Hitherto, only a few studies, exploring molecular mechanisms of healthy brain aging in higher vertebrates, utilized synaptosomal fractions to survey local changes in aging-related transcriptome dynamics.
View Article and Find Full Text PDFThe main pathological hallmarks of Alzheimer's disease (AD) consist of amyloid plaques and neurofibrillary tangles. Hippocampal cell loss, atrophy and cholinergic dysfunction are also features of AD. The present work is aimed at studying the interactions between cholinergic denervation, APP processing and hippocampal integrity.
View Article and Find Full Text PDFThe up-regulation of the angiogenic vascular endothelial growth factor (VEGF) in brains of Alzheimer patients in close relationship to beta-amyloid (Abeta) plaques, suggests a link of VEGF action and processing of the amyloid precursor protein (APP). To reveal whether VEGF may affect APP processing, brain slices derived from 17-month-old transgenic Tg2576 mice were exposed with 1ng/ml VEGF for 6, 24, and 72h, followed by assessing cytosolic and membrane-bound APP expression, level of both soluble and fibrillar Abeta-peptides, as well as activities of alpha- and beta-secretases in brain slice tissue preparations. Treatment of brain slices with VEGF did not significantly affect the expression level of APP, regardless of the exposure time studied.
View Article and Find Full Text PDFIncreased expression of interleukin (IL)-1beta has been found in Alzheimer brain, raising the question whether plaque-associated up-regulation of IL-1beta may contribute to neurodegeneration. IL-1beta is capable to induce a number of events that also occur in Alzheimer's disease such as stimulation of the amyloidogenic pathway of amyloid precursor protein processing. However, less is known on participation of IL-1beta in specific cholinergic cell loss.
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