Impacts of DNA methylation on Tau protein related genes in the brains of patients with Alzheimer’s disease

Wei, Xie-Ze; Du, Pengchong; Zhi-gang, Zhao

doi:10.1016/j.neulet.2021.136196

Cited by 5 publications

(3 citation statements)

References 61 publications

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“…It has an important association with the pathogenesis of neurodegenerative diseases; in these cases, it induces the formation of microtubules (MAP) in neurons, if it is methylated or silenced in the human brain, its activity is depressed, and in this state, it polymerizes forming abnormal neurofibrillary networks such as those found in Alzheimer's disease. 40 For context, sleep depletion can cause an increase in ROS and a decrease in antioxidants such as glutathione, leading to DNA hypomethylation and aberrant gene expression. This alteration in gene regulation does not allow the brain to function properly.…”

Section: Genetic Basismentioning

confidence: 99%

Clinical Implications and Genetic Basis of Sleep Deprivation in Children

Martínez-Torres,

Diaz-Orjuela,

Morales

et al. 2024

Journal of Child Science

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Sleep is a complex biological and physiological process that allows the body to rest in addition to playing an important role in proper homeostasis in different body systems such as immune, metabolic, cardiovascular, neurological, and hormonal. It is important to preserve the quality of sleep, for adequate vitality, since the alterations that occur in any of the phases of sleep have repercussions on several systems of an organism, whether they are short or long term, such as the negative effect of sleep deprivation on the hormonal and metabolic regulation of various pathophysiological processes that will contribute to the development of obesity in pediatric patients. It has been found that sleep-related problems are common in children, being a frequent reason for medical consultations. In addition to the aforementioned, there may also be alterations at the level of the cortex, which is associated with the nonregulation of emotions in preadolescent and adolescent pediatric patients. Finally, sleep could depend on polymorphisms that become risk alleles for having short-term sleep; likewise, there are genes that have a greater expression at the time of rest, which allows a relationship to be made with diseases developed in the face of sleep depletion. This article describes the clinical implications in pediatric patients as a consequence of sleep deprivation and its genetic bases.

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Section: Genetic Basismentioning

confidence: 99%

Clinical Implications and Genetic Basis of Sleep Deprivation in Children

Martínez-Torres,

Diaz-Orjuela,

Morales

et al. 2024

Journal of Child Science

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“…Clinicians have been looking for a way to classify MR-based imaging data (including structural MRI and rs-fMRI data) and, more significantly, to separate data from patients with brain diseases from data from healthy individuals [20][21][22]. Researchers and doctors will be aided in their quest to find a cure for Alzheimer's by the robust machine learning algorithm known as Deep Learning, which can detect brain illness [23][24]. This paper's primary contributions are as follows:…”

Section: Introductionmentioning

confidence: 99%

Ad-Tl: Alzheimer’s Disease Prediction Using Transfer Learning

Archana Gopinadhan

2024

jes

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Although many statistical methods and machine learning algorithms have been explored in both clinical and research settings to extract these patterns from neuroimaging data, differentiating between Alzheimer's disease and healthy brain data in older adults (age > 75) has proven challenging due to highly similar patterns of brain atrophy and image intensities. Medical image analysis is just one field that has benefited from the widespread use of deep learning technologies in recent years. This research paper proposed AD prediction using transfer learning (AD-TL) methods. The MRI dataset has been normalized using the Multi-Layer Perception model (MLP) with the CNN algorithm. In order to improve images, the CLAHE (Contrast-Limited Adaptive Histogram Equalization) technique has been used. Image segmentation has been done with Watershed Image segmentation. The training has been done with the Residual network (ResNet 50) with Alex net. Finally, the classification has been done with the Deep Convolutional neural network (DCNN) algorithm.According to the experimental data, the classification accuracy of the technique provided in this study may reach 99%.

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“…AD is characterised by chronic neuroinflammation, synaptic dysfunction, loss of neurons, and brain atrophy. At the molecular level, the accumulation of amyloid-beta (Aβ) peptides and tau protein tangles in neurons are some hallmark characteristics of AD, contributing significantly to the disease's pathogenesis [2][3][4][5][6][7] . However, the intricate mechanisms underlying synaptic dysfunction and subsequent neurodegeneration remain incompletely understood, hindering the development of effective therapeutics.…”

Section: Introductionmentioning

confidence: 99%

Amyloid-β can activate JNK signalling via WNT-5A/ROR2 to reduce synapse formation in Alzheimer’s disease

Fang,

Pishva,

Piers

et al. 2024

Preprint

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Wnt signalling is an essential signalling system in neurogenesis, and recent studies have highlighted the critical role of this signalling network in regulating synaptic plasticity, neuronal survival, and neurogenesis, processes that are disrupted in Alzheimer’s disease (AD). From the Wnt network, the Wnt/β-catenin pathway has been studied for its neuroprotective role, and this is suppressed in AD. However, the involvement of the non-canonical pathway, which operates independently of β-catenin and involves the planar cell polarity (PCP), remains to be determined in AD.In this work, we analyse the function of the orphan receptor tyrosine kinase ROR2, an essential co-receptor of the Wnt/PCP signalling pathway. We find that activation of WNT-5A/ROR2 signalling activates JNK signalling, reducing pre- and postsynaptic clusters on neurites in mature SH-SY5Y neurons. This observation is similar to SH-SY5Y neurons treated with the Amyloid-β peptide Aβ1-42or DKK1, which are both increased in AD. Surprisingly, the effect of Aβ1-42and DKK1 signalling on synaptogenesis can be mitigated by blocking ROR2 and JNK signalling, suggesting that Aβ and DKK1 signalling depends on ROR2/JNK signalling. Finally, we find an increase of WNT-5A/ROR2 clusters on neurites of iPSC-derived cortical neurons carrying the PSEN1 A75V mutation, known to enhance the pathological Aβ42/40ratio. Simultaneously, the number of pre- and post-synaptic clusters decreased in the mutant line. Inhibition of ROR2/JNK signalling in PSEN1A75Vcortical neurons partially rescues the reduction in synaptogenesis, suggesting that ROR2 signalling may act in a positive feedback loop with Aβ1-42and DKK1 signalling to augment JNK signalling as seen in AD.

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Impacts of DNA methylation on Tau protein related genes in the brains of patients with Alzheimer’s disease

Cited by 5 publications

References 61 publications

Clinical Implications and Genetic Basis of Sleep Deprivation in Children

Clinical Implications and Genetic Basis of Sleep Deprivation in Children

Ad-Tl: Alzheimer’s Disease Prediction Using Transfer Learning

Amyloid-β can activate JNK signalling via WNT-5A/ROR2 to reduce synapse formation in Alzheimer’s disease

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