Symptomatic, Genetic, and Mechanistic Overlaps between Autism and Alzheimer’s Disease

Nadeem, Muhammad Shahid; Hosawi, Salman; Alshehri, Sultan; Ghoneim, Mohammed M.; Imam, Syed Sarim; Murtaza, Bibi Nazia; Kazmi, Imran

doi:10.3390/biom11111635

Cited by 27 publications

(12 citation statements)

References 234 publications

(214 reference statements)

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“…In another study, PTPRD was identified as the significant gene associated with AD [ 29 ]. The MACROD2 , which was the neurodevelopmental-related gene, was reported as the risk loci of autism spectrum disorder [ 30 ], while the autism spectrum disorder had overlapping mechanisms of pathogenesis with AD [ 31 ]. Therefore, we suggested that the MACROD2 was associated with AD by affecting the autism spectrum disorder.…”

Section: Discussionmentioning

confidence: 99%

Detection of Association Features Based on Gene Eigenvalues and MRI Imaging Using Genetic Weighted Random Forest

Wang

Meng

et al. 2022

Genes

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In the studies of Alzheimer’s disease (AD), jointly analyzing imaging data and genetic data provides an effective method to explore the potential biomarkers of AD. AD can be separated into healthy controls (HC), early mild cognitive impairment (EMCI), late mild cognitive impairment (LMCI) and AD. In the meantime, identifying the important biomarkers of AD progression, and analyzing these biomarkers in AD provide valuable insights into understanding the mechanism of AD. In this paper, we present a novel data fusion method and a genetic weighted random forest method to mine important features. Specifically, we amplify the difference among AD, LMCI, EMCI and HC by introducing eigenvalues calculated from the gene p-value matrix for feature fusion. Furthermore, we construct the genetic weighted random forest using the resulting fused features. Genetic evolution is used to increase the diversity among decision trees and the decision trees generated are weighted by weights. After training, the genetic weighted random forest is analyzed further to detect the significant fused features. The validation experiments highlight the performance and generalization of our proposed model. We analyze the biological significance of the results and identify some significant genes (CSMD1, CDH13, PTPRD, MACROD2 and WWOX). Furthermore, the calcium signaling pathway, arrhythmogenic right ventricular cardiomyopathy and the glutamatergic synapse pathway were identified. The investigational findings demonstrate that our proposed model presents an accurate and efficient approach to identifying significant biomarkers in AD.

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Section: Discussionmentioning

confidence: 99%

Detection of Association Features Based on Gene Eigenvalues and MRI Imaging Using Genetic Weighted Random Forest

Wang

Meng

et al. 2022

Genes

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“…Evidence reports that neurodegenerative disease is more prevalent in adults with ASD (148). Alzheimer's disease (AD) is a neurodegenerative disease that has similar mechanisms supporting the pathogenesis of ASD (149). A key protein implicated in the pathology of AD is amyloid precursor protein (APP).…”

Section: Inflammatory and Immune Disease Associated With Autism Spect...mentioning

confidence: 99%

Neuronal Cell Adhesion Molecules May Mediate Neuroinflammation in Autism Spectrum Disorder

et al. 2022

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Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by restrictive and repetitive behaviors, alongside deficits in social interaction and communication. The etiology of ASD is largely unknown but is strongly linked to genetic variants in neuronal cell adhesion molecules (CAMs), cell-surface proteins that have important roles in neurodevelopment. A combination of environmental and genetic factors are believed to contribute to ASD pathogenesis. Inflammation in ASD has been identified as one of these factors, demonstrated through the presence of proinflammatory cytokines, maternal immune activation, and activation of glial cells in ASD brains. Glial cells are the main source of cytokines within the brain and, therefore, their activity is vital in mediating inflammation in the central nervous system. However, it is unclear whether the aforementioned neuronal CAMs are involved in modulating neuroimmune signaling or glial behavior. This review aims to address the largely unexplored role that neuronal CAMs may play in mediating inflammatory cascades that underpin neuroinflammation in ASD, primarily focusing on the Notch, nuclear factor-κB (NF-κB), and mitogen-activated protein kinase (MAPK) cascades. We will also evaluate the available evidence on how neuronal CAMs may influence glial activity associated with inflammation. This is important when considering the impact of environmental factors and inflammatory responses on ASD development. In particular, neural CAM1 (NCAM1) can regulate NF-κB transcription in neurons, directly altering proinflammatory signaling. Additionally, NCAM1 and contactin-1 appear to mediate astrocyte and oligodendrocyte precursor proliferation which can alter the neuroimmune response. Importantly, although this review highlights the limited information available, there is evidence of a neuronal CAM regulatory role in inflammatory signaling. This warrants further investigation into the role other neuronal CAM family members may have in mediating inflammatory cascades and would advance our understanding of how neuroinflammation can contribute to ASD pathology.

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“…It is the most common cause of dementia, memory loss, depression and language impairments [ 136 ]. The main causes of AD include accumulation of amyloid β (Aβ) in the form of plaques [ 137 ], or deposition of Tau protein in the neurological tissues [ 138 ]. Declined levels of neurotransmitter acetylcholine (Ach) by the action of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) also result in the onset of AD.…”

Section: Allicin As a Neuroprotective Agent To Fight Against Neurological Diseasesmentioning

confidence: 99%

Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment

et al. 2021

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Allicin (diallylthiosulfinate) is a defense molecule produced by cellular contents of garlic (Allium sativum L.). On tissue damage, the non-proteinogenic amino acid alliin (S-allylcysteine sulfoxide) is converted to allicin in an enzyme-mediated process catalysed by alliinase. Allicin is hydrophobic in nature, can efficiently cross the cellular membranes and behaves as a reactive sulfur species (RSS) inside the cells. It is physiologically active molecule with the ability to oxidise the thiol groups of glutathione and between cysteine residues in proteins. Allicin has shown anticancer, antimicrobial, antioxidant properties and also serves as an efficient therapeutic agent against cardiovascular diseases. In this context, the present review describes allicin as an antioxidant, and neuroprotective molecule that can ameliorate the cognitive abilities in case of neurodegenerative and neuropsychological disorders. As an antioxidant, allicin fights the reactive oxygen species (ROS) by downregulation of NOX (NADPH oxidizing) enzymes, it can directly interact to reduce the cellular levels of different types of ROS produced by a variety of peroxidases. Most of the neuroprotective actions of allicin are mediated via redox-dependent pathways. Allicin inhibits neuroinflammation by suppressing the ROS production, inhibition of TLR4/MyD88/NF-κB, P38 and JNK pathways. As an inhibitor of cholinesterase and (AChE) and butyrylcholinesterase (BuChE) it can be applied to manage the Alzheimer’s disease, helps to maintain the balance of neurotransmitters in case of autism spectrum disorder (ASD) and attention deficit hyperactive syndrome (ADHD). In case of acute traumatic spinal cord injury (SCI) allicin protects neuron damage by regulating inflammation, apoptosis and promoting the expression levels of Nrf2 (nuclear factor erythroid 2-related factor 2). Metal induced neurodegeneration can also be attenuated and cognitive abilities of patients suffering from neurological diseases can be ameliorates by allicin administration.

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Symptomatic, Genetic, and Mechanistic Overlaps between Autism and Alzheimer’s Disease

Cited by 27 publications

References 234 publications

Detection of Association Features Based on Gene Eigenvalues and MRI Imaging Using Genetic Weighted Random Forest

Detection of Association Features Based on Gene Eigenvalues and MRI Imaging Using Genetic Weighted Random Forest

Neuronal Cell Adhesion Molecules May Mediate Neuroinflammation in Autism Spectrum Disorder

Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment

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