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      Prognosis of Biomarker of Alzheimer's Disease in the Function of the Retina and Secondary Molecular Structure Variation of the Retina and Brain

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          Abstract

          Alzheimer's disease (AD) is one of the most serious neurodegenerative diseases in the globe. As a result, there is an acute need to discover indications that allow for early disease detection. There is growing scientific data showing the similarities between the eye and other central nervous system components, suggesting that information obtained in ophthalmic research might be valuable in the study and diagnosis of AD. Fifty male albino Wistar rats were separated into five groups: the first group served as control, and the other four groups of animals were administrated aluminium chloride (AlCl 3) in a dose of 100 mg/kg body weight (b.w.) for 2, 4, 6, and 8 weeks, respectively. Insights into the function of the retina by electroretinogram (ERG) and the changes thought to have occurred in the molecular structure of the retina and brain using Fourier transform infrared spectroscopy (FTIR) as a result of AD progression induced by AlCl 3 in rats were done. Moreover, the measurement of acetylcholinesterase (AchE) was done. After 6 and 8 weeks of AlCl 3 injection, there was a substantial reduction ( p ≤ 0.05) in a- and b-wave amplitudes and a significant rise ( p ≤ 0.05) in implicit time compared to controls. A significant elevation ( p ≤ 0.05) of AchE content was observed after 4, 6, and 8 weeks. FTIR revealed a significant increase ( p ≤ 0.05) of β-turn and β-sheet content associated with significant decrease ( p ≤ 0.05) of α-helix content for all groups administrated with AlCl 3. Our findings suggest that retinal biomarkers such as ERG of the retina may be used as a screening tool for detection of AD. Secondary structural changes in the proteins of the retina and the brain were similar in AD rats' model and precede retinal dysfunction.

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          Inflammation as a central mechanism in Alzheimer's disease

          Jefferson Kinney, Shane M. Bemiller, Andrew S Murtishaw … (2018)
          Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles. Over the last decade, the presence of a sustained immune response in the brain has emerged as a third core pathology in AD. The sustained activation of the brain's resident macrophages (microglia) and other immune cells has been demonstrated to exacerbate both amyloid and tau pathology and may serve as a link in the pathogenesis of the disorder. In the following review, we provide an overview of inflammation in AD and a detailed coverage of a number of microglia-related signaling mechanisms that have been implicated in AD. Additional information on microglia signaling and a number of cytokines in AD are also reviewed. We also review the potential connection of risk factors for AD and how they may be related to inflammatory mechanisms.
          Article 0 comments Cited 512 times – based on 0 reviews     Review now
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            Oxidative stress: A major pathogenesis and potential therapeutic target of antioxidative agents in Parkinson's disease and Alzheimer's disease.

            Tianfang Jiang, Qian Sun, Shengdi Chen (2016)
            Oxidative stress reflects an imbalance between the overproduction and incorporation of free radicals and the dynamic ability of a biosystem to detoxify reactive intermediates. Free radicals produced by oxidative stress are one of the common features in several experimental models of diseases. Free radicals affect both the structure and function of neural cells, and contribute to a wide range of neurodegenerative diseases, including Parkinson's disease and Alzheimer's disease. Although the precise mechanisms that result in the degeneration of neurons and the relevant pathological changes remain unclear, the crucial role of oxidative stress in the pathogenesis of neurodegenerative diseases is associated with several proteins (such as α-synuclein, DJ-1, Amyloid β and tau protein) and some signaling pathways (such as extracellular regulated protein kinases, phosphoinositide 3-kinase/Protein Kinase B pathway and extracellular signal-regulated kinases 1/2) that are tightly associated with the neural damage. In this review, we present evidence, gathered over the last decade, concerning a variety of pathogenic proteins, their important signaling pathways and pathogenic mechanisms associated with oxidative stress in Parkinson's disease and Alzheimer's disease. Proper control and regulation of these proteins' functions and the related signaling pathways may be a promising therapeutic approach to the patients. We also emphasizes antioxidative options, including some new neuroprotective agents that eliminate excess reactive oxygen species efficiently and have a certain therapeutic effect; however, controversy surrounds some of them in terms of the dose and length of therapy. These agents require further investigation by clinical application in patients suffering Parkinson's disease and Alzheimer's disease.
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              Retinal amyloid pathology and proof-of-concept imaging trial in Alzheimer’s disease

              Shawn Kile, Yosef Koronyo, David Biggs … (2017)
              BACKGROUND. Noninvasive detection of Alzheimer’s disease (AD) with high specificity and sensitivity can greatly facilitate identification of at-risk populations for earlier, more effective intervention. AD patients exhibit a myriad of retinal pathologies, including hallmark amyloid β-protein (Aβ) deposits. METHODS. Burden, distribution, cellular layer, and structure of retinal Aβ plaques were analyzed in flat mounts and cross sections of definite AD patients and controls ( n = 37). In a proof-of-concept retinal imaging trial ( n = 16), amyloid probe curcumin formulation was determined and protocol was established for retinal amyloid imaging in live patients. RESULTS. Histological examination uncovered classical and neuritic-like Aβ deposits with increased retinal Aβ 42 plaques (4.7-fold; P = 0.0063) and neuronal loss ( P = 0.0023) in AD patients versus matched controls. Retinal Aβ plaque mirrored brain pathology, especially in the primary visual cortex ( P = 0.0097 to P = 0.0018; Pearson’s r = 0.84–0.91). Retinal deposits often associated with blood vessels and occurred in hot spot peripheral regions of the superior quadrant and innermost retinal layers. Transmission electron microscopy revealed retinal Aβ assembled into protofibrils and fibrils. Moreover, the ability to image retinal amyloid deposits with solid-lipid curcumin and a modified scanning laser ophthalmoscope was demonstrated in live patients. A fully automated calculation of the retinal amyloid index (RAI), a quantitative measure of increased curcumin fluorescence, was constructed. Analysis of RAI scores showed a 2.1-fold increase in AD patients versus controls ( P = 0.0031). CONCLUSION. The geometric distribution and increased burden of retinal amyloid pathology in AD, together with the feasibility to noninvasively detect discrete retinal amyloid deposits in living patients, may lead to a practical approach for large-scale AD diagnosis and monitoring. FUNDING. National Institute on Aging award (AG044897) and The Saban and The Marciano Family Foundations. Amyloid deposits in retinas of live patients were detected and quantified using curcumin and a noninvasive optical imaging technology.
              Article 0 comments Cited 118 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Eman Mohamed Aly:
                ORCID: https://orcid.org/0000-0003-0815-3063
                Journal
                Journal ID (nlm-ta): Int J Alzheimers Dis
                Journal ID (iso-abbrev): Int J Alzheimers Dis
                Journal ID (publisher-id): ijad
                Title: International Journal of Alzheimer's Disease
                Publisher: Hindawi
                ISSN (Print): 2090-8024
                ISSN (Electronic): 2090-0252
                Publication date Collection: 2023
                Publication date (Electronic): 29 March 2023
                Volume: 2023
                Electronic Location Identifier: 9775921
                Affiliations
                1Biophysics and Laser Science Unit, Visual Science Department, Research Institute of Ophthalmology, Giza, Egypt
                2Ophthalmology Department, Research Institute of Ophthalmology, Giza, Egypt
                3Biophysics Department, Science College, Ain Shams University, Cairo, Egypt
                Author notes

                Academic Editor: Yasushi Kishimoto

                Author information
                https://orcid.org/0000-0003-0815-3063
                https://orcid.org/0000-0002-7371-6742
                https://orcid.org/0000-0002-3440-7760
                https://orcid.org/0000-0003-0508-5974
                Article
                DOI: 10.1155/2023/9775921
                PMC ID: 10076121
                SO-VID: 1fb865c9-267c-4d87-99a4-710c230a560a
                Copyright statement: Copyright © 2023 Heba Ahmed Gaber et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 16 December 2022
                Date revision received : 6 February 2023
                Date accepted : 15 March 2023
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Neurology
                Data availability:
                ScienceOpen disciplines: Neurology

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