Researcher:
Anwar, Mai

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Mai

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Anwar

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Anwar, Mai

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2021 - 20224

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Researcher Of Publications: search.filters.isAuthorOfPublication.c2924384-d922-495f-b2d1-7193a65e1913

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    Oxidative stress-A direct bridge to central nervous system homeostatic dysfunction and Alzheimer's disease
    (Wiley, 2022) N/A; Anwar, Mai; Other; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; N/A
    Neurologists have highly observed a frequent increasing number of elderly patients with Alzheimer's disease (AD) without any relevant evidence of any genetic or known AD-linked predisposing factors in the past few years. Those patients are characterized by continuous and irreversible neuron cells loss along with declined cognitive functions. Numerous studies have suggested that the exaggerated release of reactive oxygen species (ROS) within the brain may develop late-onset neurodegenerative disorders, especially AD-neuroinflammatory type. However, the central nervous system is vitally linked with whole-brain chemical integrity and its related healthy state, the cascade by which ROS may result in AD's development has not been highly justified or even maintained. It is widely known that the brain consumes a vast amount of oxygen and is characterized by being rich in lipid polyunsaturated fatty acids content, explaining why it is a prone region to oxidative stress (OS) and ROS damage. The formed OS-AD cytoskeletal protein aggregates can be considered a main predisposing factor for amyloid-beta (A beta) hallmarks precipitation. Herein, this review aims to provide a detailed information on how oxidative stress can play a pathogenic role in activating damage-associated molecular patterns (DAMPs)-related toll-like receptor-4 inflammatory (TLR-4) cascades resulting in the deposition of A beta hallmarks in brain tissues ending with irreversible cognitive dysfunction. It also explains how microglia can be activated via ROS, which may significantly release several pro-inflammatory cascades ending with general brain atrophy. Furthermore, different types of suggested antioxidant therapies will be discussed to combat AD-related pathological disorders and hallmarks.
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    The therapeutic potential and efficiency of intracerebroventricular transplantation and intravenous injection of mesenchymal stem cells in relieving a beta hallmarks and improving cognitive dysfunction in ad induced model
    (Elsevier, 2021) Ali, Ola S. M.; Rashed, Laila A.; Badawi, A. M.; Eltablawy, Nadia A.; Anwar, Mai; Other; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A
    Background: Alzheimer's disease (AD) has been considered a long-lasting, devastating public health concern due to a high folding increase in global aging percentage worldwide. Different approaches have been confined to cut down this high percentage of neurodegenerative disorder due to a lack of successful, efficient strategic protocol for AD treatment. One of these approaches is the transplantation or injection of mesenchymal stem cells (MSCs) due to their neuromodulatory, anti-inflammatory, and antioxidant actions. Aim: To elucidate and determine whether intravenous (IV) or intracerebroventricular (ICV) administration of MSCs is the most efficient and successful method in engulfing amyloid-beta plaques and improving cognitive defects. Material and methods: The efficiency of MSCs was investigated on lipopolysaccharides (LPS) AD-induced rats. Thirty-two rats were randomly divided equally into four groups identified as a control group (C/G1), AD-induced group (AD/G2), intravenous AD-induced group (IV/G3), and ICV AD-induced group (ICV/G4). Amyloid-beta, tau protein, tumor necrosis factor-alpha (TNF-alpha), interleukin (IL-10) were detected using the ELISA technique while MDA and GSH brain tissue level were detected colorimetry. Results: The histopathological examination of different brain tissues demonstrated the presence of A beta plaques following LPS induction. Administration of both types of MSCs into AD-induced rats resulted in a significant decrease in the brain's hallmarks depositions, oxidative stress, and inflammatory factors with different degrees and efficiency. Conclusion: The present study indicates the efficiency of both types of MSCs administration in improving AD subjects' cognitive defects with a more relevant efficiency following ICV administration, considering the risk to benefits ratio before taking inaction treatment initiation.
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    Brain-printing biometrics underlying mechanism as an early diagnostic technique for Alzheimer's disease neurodegenerative type
    (Elsevier B.V., 2021) N/A; Anwar, Mai; Other; N/A; N/A
    Early diagnosis of neurodegenerative diseases, especially Alzheimer's disease (AD), is essential for implementing the appropriate treatment protocols and controlling disease progression. Early AD diagnosis helps patients achieve the best therapeutic outcomes, lessening irreversible neurodegenerative damage and severe cognitive decline. The measurement of brain waves and structural modifications, including gray/white matter and brain volume, have recently been considered a promising approach for brain biometrics because of the inherent specificity, degree of confidentiality, and reproducibility. Brain printing biometrics (BPB) is thus becoming more commonly considered as tool for early AD detection. This review proposes using BPB as a tool for the detection of AD prior to the appearance of persistent hallmark depositions, including Aβ and tau protein aggregations in different brain regions. It also describes BPB authentication, a method of implementation, as well as potential outcomes.
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    The role of Extracellular Matrix alterations in mediating Astrocytes damage, and Pericytes dysfunction in Alzheimer's disease: a comprehensive review
    (Wiley, 2022) N/A; N/A; N/A; Anwar, Mai; Özkan, Esra; Özdemir, Yasemin Gürsoy; Other; Researcher; Faculty Member; Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); Koç University Research Center for Translational Medicine (KUTTAM) / Koç Üniversitesi Translasyonel Tıp Araştırma Merkezi (KUTTAM); N/A; N/A; School of Medicine; N/A; N/A; 170592
    The brain is a highly vascularized tissue protected by the blood-brain barrier (BBB), a complex structure allowing only necessary substances to pass through into the brain while limiting the entrance of harmful toxins. The BBB comprises several components, and the most prominent features are tight junctions between endothelial cells (ECs), which are further wrapped in a layer of pericytes. Pericytes are multitasked cells embedded in a thick basement membrane (BM) that consists of a fibrous extracellular matrix (ECM) and are surrounded by astrocytic endfeet. The primary function of astrocytes and pericytes is to provide essential blood supply and vital nutrients to the brain. In Alzheimer's disease (AD), long-term neuroinflammatory cascades associated with infiltration of harmful neurotoxic proteins may lead to BBB dysfunction and altered ECM components resulting in brain homeostatic imbalance, synaptic damage, and declined cognitive functions. Moreover, BBB structure and functional integrity may be lost due to induced ECM alterations, astrocyte damage, and pericytes dysfunction, leading to amyloid-beta (A beta) hallmarks deposition in different brain regions. Herein, we highlight how BBB, ECM, astrocytes, and pericytes dysfunction can play a leading role in AD's pathogenesis and discuss their impact on brain functions.