A study on the amyloid toxicity in Alzheimer’s disease model of APPL-Gal4 Drosophila eye

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This study utilized the APPL-Gal4 Drosophila eye model to investigate amyloid-beta aggregation pathology relevant to Alzheimer's disease and explore potential therapeutic drug discovery insights.

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The preprint investigates amyloid-beta (Aβ42) toxicity in a Drosophila Alzheimer’s disease model by misexpressing human Aβ42 in the developing eye using an eye-specific APPL-Gal4 system, with comparisons to wild-type controls. Transgenic flies exhibited eye degeneration characterized by disrupted ommatidial structure, reduced eye size, pigmentation loss, and photoreceptor abnormalities, as assessed by SEM imaging and histology (H-E staining) of 4-µm paraffin sections; the study also reports that sra overexpression aggravated the Aβ42-associated rough-eye phenotype, while sra alone produced only slight roughening. The authors’ primary limitation is that the work is a preprint and, in the provided text, focuses mainly on morphological readouts rather than mechanistic or quantitative molecular endpoints. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disorders. The pathogenesis involves two hallmarks: amyloid-beta aggregation (Aβ) and neurofibrillary tangles (NFTs). This has incited the use of animal models to mirror the disease. The fruit fly, Drosophila melanogaster has garnered considerable attention as an organism to recapitulate human disorders. Drosophilaisusedas novel genetic tools for studying cellular aspects and behavioural and physiological traits of human neurodegenerative diseases. Here, authors use the Drosophila model in understanding AD pathology and the insights were gained in drug discovery for AD therapy
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A study on the amyloid toxicity in Alzheimer’s disease model of APPL-Gal4 Drosophila eye | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Method Article A study on the amyloid toxicity in Alzheimer’s disease model of APPL-Gal4 Drosophila eye Pratap G.K., Manjula Shantaram This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-463150/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disorders. The pathogenesis involves two hallmarks: amyloid-beta aggregation (Aβ) and neurofibrillary tangles (NFTs). This has incited the use of animal models to mirror the disease. The fruit fly, Drosophila melanogaster has garnered considerable attention as an organism to recapitulate human disorders. Drosophilaisusedas novel genetic tools for studying cellular aspects and behavioural and physiological traits of human neurodegenerative diseases. Here, authors use the Drosophila model in understanding AD pathology and the insights were gained in drug discovery for AD therapy Neurobiology of Disease Drosophila melanogaster Alzheimer’s disease Figures Figure 1 Introduction Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disorders. The pathogenesis involves two hallmarks: amyloid-betaaggregation (Aβ) and neurofibrillary tangles (NFTs). This has incited the use of animal models to mirror the disease. The fruit fly, Drosophila melanogaster has garnered considerable attention as an organism to recapitulate human disorders. Drosophila is usedas novel genetic tools for studying not only cellular aspects but alsobehavioural andphysiological traits of human neurodegenerative diseases. Here, authors use the Drosophila model in understanding AD pathology and the insights were gained in drug discovery for AD therapy[1]. Nearly 75% of human genes linked with the disease have a Drosophila ortholog, hence Drosophila is theultimate model to study neurodegenerative diseases [2]. D. melanogaster eye has a red-brown colour caused by the presence of two pigments, pteridines (red),ommochromes (brown) and it contains a set of mechano-sensory bristles, which are to be found at the anterior vertex of each ommatidium[3]. It consists of eight(8) photoreceptor cells and support cells. The AD model amenability of the Gal4/UAS targeted system allows misexpression of foreign genes along the spatiotemporal axes in the developing Drosophila eye. AD model system in Drosophila eye increased the levels of human amyloid-beta (Aβ42) which was mis-expressed in the differentiating retinal neurons of the developing fly retina using a Glass Multiple Repeat Gal4 driver[4]. The transgenic flies model exhibited strong neurodegeneration in the fly retina and resultedin reduced eye size. Objectives To study Aβ toxicity in Alzheimer's disease model of APPL-Gal4 eye Materials And Methods Transgenic APPL-Gal4 model (45 days’ old) Control model Wild type Drosophila (Oregon K) APPL-Gal-4 flies' eyes were observed under SEM(SEM images showed a distinct pattern of eye degeneration in the eye context) Histopathology: The flies were anaesthetised, fixed in Carnoy’s fixativeat4°C overnight. After the fixation of the flies’ heads, the fly sample was dehydrated in alcohol (40-100%) and the heads were embedded in paraffin wax. Sections of 4µm thick heads were stained with H-E stain[5]. The stained fly sections were observed under a light microscope (Olympus) for neuroanatomical studies to confirm the internal morphology of the flies’ eye sections, which showed loss of bristle, disrupted ommatidial reduced eye size and photoreceptor abnormalities in the eye. Results/ Observations Control eye (Wild type; A)- No disruption in eye morphology and no loss of corneal lenses (ommatidia) (B) Transgenic APPL-GAL4 eye when Aβ expressed in eye tissue showing loss of eye morphology and corneal lenses. Using an eye specific GAL4 driver, the AD gene was expressed in the eye. The AD model eye was compared with the normal(Wild type Drosophila)eye, the degenerative eye can show disruption of ommatidial structure, reduced size, and loss of pigmentation (Fig.1) [6] The eye phenotypes influencedby abnormal expression of Aβ42 in the developing eye were aggravated by sra overexpression. The overexpressing of Aβ42 in the adult eye has severely distorted nerve tissue as a result of neurodegeneration. Overexpression of sra alone resulted in a slightly rougheye compared with that of the control eye. Overexpression of sra in Aβ42-expressing flies exacerbated the rough-eye phenotype (H-J) for this reason we used APPL-Gal4 fly models for AD. Conclusion The Drosophila melanogaster is one of the best model to study human disorders. There are currently different Drosophila models for neurodegenerative diseases studies including Huntington's disease, parkinson's disease, motor neuron disease, and AD. There are many distinct fly models for a range of neurodegenerative diseases; we focus on select studies from models of APPL-Gal4. These fly models, providing understanding into Aβ expressed in eye tissue, studying the eye morphology, corneal lenses, mechanisms and pathways, as a foundation for translational and therapeutic research. Declarations Competing interests The authors declare no competing interests. References [1] Tan FHP, Azzam G. Drosophila melanogaster: Deciphering Alzheimer’s disease. Malaysian J Med Sci 2017;24:6–20. https://doi.org/10.21315/mjms2016.24.2.2. [2] Pandey UB, Nichols CD. Human disease models in drosophila melanogaster and the role of the fly in therapeutic drug discovery. Pharmacol Rev 2011;63:411–36. https://doi.org/10.1124/pr.110.003293. [3] Loscalzo DEHRCJ. Building an Ommatidium One Cell at a Time. Bone 2011;23:1–7. https://doi.org/10.1002/dvdy.23707.Building. [4] Cutler T, Sarkar A, Moran M, Steffensmeier A, Puli OR, Mancini G, et al. Drosophila eye model to study neuroprotective role of CREB binding protein (CBP) in Alzheimer’s disease. PLoS One 2015;10:1–18. https://doi.org/10.1371/journal.pone.0137691. [5] Kucherenko MM, Marrone AK, Rishko VM, Yatsenko AS, Klepzig A, Shcherbata HR. Paraffin-Embedded and Frozen Sections of Drosophila Adult Muscles. J Vis Exp 2010. https://doi.org/10.3791/2438. [6] McGurk L, Berson A, Bonini NM. Drosophila as an in vivo model for human neurodegenerative disease. Genetics 2015;201:377–402. https://doi.org/10.1534/genetics.115.179457. [7] Lee S, Bang SM, Hong YK, Lee JH, Jeong H, Hwan S. The calcineurin inhibitor , Sarah / Nebula , exacerbates A 42 phenotypes in a Drosophila model of Alzheimer’s disease 2015. https://doi.org/10.1242/dmm.018069. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-463150","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Method Article","associatedPublications":[],"authors":[{"id":23261823,"identity":"456393a0-2855-40e9-b2a3-f5e8bb24a536","order_by":0,"name":"Pratap G.K.","email":"","orcid":"","institution":"Mangalore University","correspondingAuthor":false,"prefix":"","firstName":"Pratap","middleName":"","lastName":"G.K.","suffix":""},{"id":23261824,"identity":"b05d263c-a9a7-4a59-8fb7-f35f7e039bc1","order_by":1,"name":"Manjula Shantaram","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA20lEQVRIiWNgGAWjYJACA4YChnp+9gYQ04JYLQYMCZI9B0BMCeLtSTC4kQBiEaFFt/3sgWIeA7s8g5vPr274USDBwN/enYBXi9mZvARjHoPkYsnbOWU3e4AOkzhzdgN+LQdyDIBamBn7buek3eABajGQyCWg5fwbkJZ6xoabZ9Ju/iFKyw2wLYcTJ9xgP3abOFtuvDEwnGNw3FiyJ4fttoyBBA9hv5zPMTN4U1Etx89+/NnNN39s5Pjbe/FrAQI2AwjNA6Z5CCkHAeYHEJr9ATGqR8EoGAWjYAQCAOaPR0vBm6tmAAAAAElFTkSuQmCC","orcid":"","institution":"Mangalore University","correspondingAuthor":true,"prefix":"","firstName":"Manjula","middleName":"","lastName":"Shantaram","suffix":""}],"badges":[],"createdAt":"2021-04-26 04:31:17","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-463150/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-463150/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":8782579,"identity":"9db82377-a94f-4552-9aac-42e206645718","added_by":"auto","created_at":"2021-05-04 23:19:27","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":108696,"visible":true,"origin":"","legend":"Control eye (Wild type; A1 Microscopic image A2: SEM image and A3 Histopathology)- No disruption in eye morphology and no loss of corneal lenses (ommatidia).Transgenic APPL-GAL4 eye(B1 Microscopic image B2: SEM image and B3 Histopathology), when Aβ expressed in eye tissue, showed loss of eye morphology and corneal lenses(B2 and B3).","description":"","filename":"Picturep1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-463150/v1/962e7258a99c89c7725bf8ef.jpg"},{"id":13691835,"identity":"c0273229-d75e-469c-b125-550b4cad5c0a","added_by":"auto","created_at":"2021-09-17 12:40:13","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":274904,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-463150/v1/ef724709-122d-4be9-8e21-b3902c4f25ff.pdf"}],"financialInterests":"","formattedTitle":"\u003cp\u003eA study on the amyloid toxicity in Alzheimer’s disease model of APPL-Gal4 Drosophila eye\u003c/p\u003e\u003cp\u003e\u003cbr\u003e\u003c/p\u003e","fulltext":[{"header":"Introduction","content":"\u003cp\u003eAlzheimer\u0026rsquo;s disease (AD) is one of the most prevalent neurodegenerative disorders. The pathogenesis involves two hallmarks: amyloid-betaaggregation (A\u0026beta;) and neurofibrillary tangles (NFTs). This has incited the use of animal models to mirror the disease. The fruit fly,\u0026nbsp;\u003cem\u003eDrosophila melanogaster\u003c/em\u003e\u0026nbsp;has garnered considerable attention as an organism to recapitulate human disorders. \u003cem\u003eDrosophila\u003c/em\u003e\u003cem\u003eis\u003c/em\u003e\u003cem\u003eusedas novel genetic tools \u003c/em\u003efor studying not only cellular aspects but alsobehavioural andphysiological traits of human neurodegenerative diseases. Here, authors use the\u0026nbsp;\u003cem\u003eDrosophila\u003c/em\u003e\u0026nbsp;model in understanding AD pathology and the insights were gained in drug discovery for AD therapy[1].\u003c/p\u003e\n\u003cp\u003eNearly 75% of human genes linked with the disease have a\u0026nbsp;\u003cem\u003eDrosophila\u003c/em\u003e\u0026nbsp;ortholog, hence\u0026nbsp;\u003cem\u003eDrosophila\u003c/em\u003e\u0026nbsp;is theultimate model to study neurodegenerative diseases [2].\u003cem\u003eD. melanogaster\u003c/em\u003eeye has a red-brown colour caused by the presence of two pigments, pteridines (red),ommochromes (brown) and it contains a set of mechano-sensory bristles, which are to be found at the anterior vertex of each ommatidium[3]. It consists of eight(8) photoreceptor cells and support cells. The AD model amenability of the Gal4/UAS targeted system allows misexpression of foreign genes along the spatiotemporal axes in the developing\u003cem\u003eDrosophila\u003c/em\u003e eye. AD model system in\u0026nbsp;\u003cem\u003eDrosophila\u003c/em\u003e\u0026nbsp;eye increased the levels of human amyloid-beta (A\u0026beta;42) which was mis-expressed in the differentiating retinal neurons of the developing fly retina using a Glass Multiple Repeat Gal4 driver[4]. The transgenic flies model exhibited strong neurodegeneration in the fly retina and resultedin reduced eye size.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eObjectives\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eTo study A\u0026beta; toxicity in Alzheimer's disease model of APPL-Gal4 eye\u003c/p\u003e"},{"header":"Materials And Methods","content":"\u003col\u003e\n\u003cli\u003eTransgenic APPL-Gal4 model (45 days\u0026rsquo; old)\u003c/li\u003e\n\u003cli\u003eControl model Wild type Drosophila (Oregon K)\u003c/li\u003e\n\u003cli\u003eAPPL-Gal-4 flies' eyes were observed under SEM(SEM images showed a distinct pattern of eye degeneration in the eye context)\u003c/li\u003e\n\u003cli\u003eHistopathology: The flies were anaesthetised, fixed in Carnoy\u0026rsquo;s fixativeat4\u0026deg;C overnight. After the fixation of the flies\u0026rsquo; heads, the fly sample was dehydrated in alcohol (40-100%) and the heads were embedded in paraffin wax. Sections of 4\u0026micro;m thick heads were stained with H-E stain[5]. The stained fly sections were observed under a light microscope (Olympus) for neuroanatomical studies to confirm the internal morphology of the flies\u0026rsquo; eye sections, which showed loss of bristle, disrupted ommatidial reduced eye size and photoreceptor abnormalities in the eye.\u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Results/ Observations","content":"\u003cp\u003eControl eye \u003cstrong\u003e(Wild type; A)-\u003c/strong\u003e No disruption in eye morphology and no loss of corneal lenses (ommatidia) \u003cstrong\u003e(B)\u003c/strong\u003eTransgenic APPL-GAL4 eye when A\u0026beta; expressed in eye tissue showing loss of eye morphology and corneal lenses. Using an eye specific GAL4 driver, the AD gene was expressed in the eye. The AD model eye was compared with the normal(Wild type Drosophila)eye, the degenerative eye can show disruption of ommatidial structure, reduced size, and loss of pigmentation\u003cstrong\u003e(Fig.1)\u003c/strong\u003e[6]\u003c/p\u003e\n\u003cp\u003eThe eye phenotypes influencedby abnormal expression of A\u0026beta;42 in the developing eye were aggravated by \u003cem\u003esra\u003c/em\u003e overexpression. The overexpressing of A\u0026beta;42 in the adult eye has severely distorted nerve tissue as a result of neurodegeneration. Overexpression of \u003cem\u003esra\u003c/em\u003e alone resulted in a slightly rougheye compared with that of the control eye. Overexpression of \u003cem\u003esra\u003c/em\u003e in A\u0026beta;42-expressing flies exacerbated the rough-eye phenotype (H-J) for this reason we used APPL-Gal4 fly models for AD.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThe \u003cem\u003eDrosophila melanogaster\u003c/em\u003e is one of the best model to study human disorders. There are currently different Drosophila models for neurodegenerative diseases studies including Huntington's disease, parkinson's disease, motor neuron disease, and AD. There are many distinct fly models for a range of neurodegenerative diseases; we focus on select studies from models of APPL-Gal4. These fly models, providing understanding into A\u0026beta; expressed in eye tissue, studying the eye morphology, corneal lenses, mechanisms and pathways, as a foundation for translational and therapeutic research.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare no competing interests.\u003c/p\u003e"},{"header":"References","content":"\u003cp\u003e[1]\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp; Tan FHP, Azzam G. Drosophila melanogaster: Deciphering Alzheimer\u0026rsquo;s disease. Malaysian J Med Sci 2017;24:6\u0026ndash;20. https://doi.org/10.21315/mjms2016.24.2.2.\u003c/p\u003e\n\u003cp\u003e[2]\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp; Pandey UB, Nichols CD. Human disease models in drosophila melanogaster and the role of the fly in therapeutic drug discovery. Pharmacol Rev 2011;63:411\u0026ndash;36. https://doi.org/10.1124/pr.110.003293.\u003c/p\u003e\n\u003cp\u003e[3]\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp; Loscalzo DEHRCJ. Building an Ommatidium One Cell at a Time. Bone 2011;23:1\u0026ndash;7. https://doi.org/10.1002/dvdy.23707.Building.\u003c/p\u003e\n\u003cp\u003e[4]\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp; Cutler T, Sarkar A, Moran M, Steffensmeier A, Puli OR, Mancini G, et al. Drosophila eye model to study neuroprotective role of CREB binding protein (CBP) in Alzheimer\u0026rsquo;s disease. PLoS One 2015;10:1\u0026ndash;18. https://doi.org/10.1371/journal.pone.0137691.\u003c/p\u003e\n\u003cp\u003e[5]\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp; Kucherenko MM, Marrone AK, Rishko VM, Yatsenko AS, Klepzig A, Shcherbata HR. Paraffin-Embedded and Frozen Sections of \u0026lt;em\u0026gt;Drosophila\u0026lt;/em\u0026gt; Adult Muscles. J Vis Exp 2010. https://doi.org/10.3791/2438.\u003c/p\u003e\n\u003cp\u003e[6]\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp; McGurk L, Berson A, Bonini NM. Drosophila as an in vivo model for human neurodegenerative disease. Genetics 2015;201:377\u0026ndash;402. https://doi.org/10.1534/genetics.115.179457.\u003c/p\u003e\n\u003cp\u003e[7]\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp;\u0026nbsp; Lee S, Bang SM, Hong YK, Lee JH, Jeong H, Hwan S. The calcineurin inhibitor , Sarah / Nebula , exacerbates A 42 phenotypes in a Drosophila model of Alzheimer\u0026rsquo;s disease 2015. https://doi.org/10.1242/dmm.018069.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Drosophila melanogaster, Alzheimer’s disease","lastPublishedDoi":"10.21203/rs.3.rs-463150/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-463150/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eAlzheimer’s disease (AD) is one of the most prevalent neurodegenerative disorders. The pathogenesis involves two hallmarks: amyloid-beta aggregation (Aβ) and neurofibrillary tangles (NFTs). This has incited the use of animal models to mirror the disease. The fruit fly,\u0026nbsp;\u003cem\u003eDrosophila melanogaster\u003c/em\u003e\u0026nbsp;has garnered considerable attention as an organism to recapitulate human disorders. \u003cem\u003eDrosophilaisusedas novel genetic tools \u003c/em\u003efor studying cellular aspects and behavioural and physiological traits of human neurodegenerative diseases. Here, authors use the\u0026nbsp;\u003cem\u003eDrosophila\u003c/em\u003e\u0026nbsp;model in understanding AD pathology and the insights were gained in drug discovery for AD therapy\u003c/p\u003e","manuscriptTitle":"A study on the amyloid toxicity in Alzheimer’s disease model of APPL-Gal4 Drosophila eye","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2021-05-04 23:19:26","doi":"10.21203/rs.3.rs-463150/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"cfedd215-b9cf-4022-9a08-80704f08239e","owner":[],"postedDate":"May 4th, 2021","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[{"id":3887119,"name":"Neurobiology of Disease"}],"tags":[],"updatedAt":"2021-05-04T23:19:26+00:00","versionOfRecord":[],"versionCreatedAt":"2021-05-04 23:19:26","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-463150","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-463150","identity":"rs-463150","version":["v1"]},"buildId":"_2-kVJe1T_tPrBINL-cwx","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}

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