ORCID Profile
0000-0003-1317-0829
Current Organisations
Menoufia University
,
International Islamic University Malaysia
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Publisher: Walter de Gruyter GmbH
Date: 20-12-2017
DOI: 10.1515/REVNEURO-2017-0036
Abstract: In this review, we discuss the genetic etiologies of Alzheimer’s disease (AD). Furthermore, we review genetic links to protein signaling pathways as novel pharmacological targets to treat AD. Moreover, we also discuss the clumps of AD-m ediated genes according to their single nucleotide polymorphism mutations. Rigorous data mining approaches justified the significant role of genes in AD prevalence. Pedigree analysis and twin studies suggest that genetic components are part of the etiology, rather than only being risk factors for AD. The first autosomal dominant mutation in the amyloid precursor protein ( APP ) gene was described in 1991. Later, AD was also associated with mutated early-onset (presenilin 1/2, PSEN1/2 and APP ) and late-onset (apolipoprotein E, ApoE ) genes. Genome-wide association and linkage analysis studies with identified multiple genomic areas have implications for the treatment of AD. We conclude this review with future directions and clinical implications of genetic research in AD.
Publisher: Medknow
Date: 2016
Publisher: Walter de Gruyter GmbH
Date: 09-2018
Publisher: Walter de Gruyter GmbH
Date: 2017
DOI: 10.1515/REVNEURO-2016-0083
Abstract: In this review, we provide an overview of the relationship between cannabis use and the development of schizophrenia, using both animal and human studies. We further discuss the potential neural mechanism that may mediate the relationship between cannabis use and schizophrenia symptoms. We finally provide clinical implications and future studies that can further elucidate the relationship between cannabis and schizophrenia.
Publisher: Walter de Gruyter GmbH
Date: 27-06-2018
DOI: 10.1515/REVNEURO-2017-0071
Abstract: Neurodegenerative diseases, such as Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, prion disease, and amyotrophic lateral sclerosis, are a dissimilar group of disorders that share a hallmark feature of accumulation of abnormal intraneuronal or extraneuronal misfolded/unfolded protein and are classified as protein misfolding disorders. Cellular and endoplasmic reticulum (ER) stress activates multiple signaling cascades of the unfolded protein response (UPR). Consequently, translational and transcriptional alterations in target gene expression occur in response directed toward restoring the ER capacity of proteostasis and reestablishing the cellular homeostasis. Evidences from in vitro and in vivo disease models indicate that disruption of ER homeostasis causes abnormal protein aggregation that leads to synaptic and neuronal dysfunction. However, the exact mechanism by which it contributes to disease progression and pathophysiological changes remains vague. Downstream signaling pathways of UPR are fully integrated, yet with erse unexpected outcomes in different disease models. Three well-identified ER stress sensors have been implicated in UPR, namely, inositol requiring enzyme 1, protein kinase RNA-activated-like ER kinase (PERK), and activating transcription factor 6. Although it cannot be denied that each of the involved stress sensor initiates a distinct downstream signaling pathway, it becomes increasingly clear that shared pathways are crucial in determining whether or not the UPR will guide the cells toward adaptive prosurvival or proapoptotic responses. We review a body of work on the mechanism of neurodegenerative diseases based on oxidative stress and cell death pathways with emphasis on the role of PERK.
No related grants have been discovered for Wael Mohamed.