Multifarious roles of mTOR signaling in cognitive aging and cerebrovascular dysfunction of Alzheimer's disease
Age‐related cognitive failure is a main devastating incident affecting even healthy people. Alzheimer's disease (AD) is the utmost common form of dementia among the geriatric community. In the pathogenesis of AD, cerebrovascular dysfunction is revealed before the beginning of the cognitive decl...
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| Veröffentlicht in: | IUBMB life 2020-09, Vol.72 (9), p.1843-1855 |
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| creator | Uddin, Md. Sahab Rahman, Md. Ataur Kabir, Md. Tanvir Behl, Tapan Mathew, Bijo Perveen, Asma Barreto, George E. Bin‐Jumah, May N. Abdel‐Daim, Mohamed M. Ashraf, Ghulam Md |
| description | Age‐related cognitive failure is a main devastating incident affecting even healthy people. Alzheimer's disease (AD) is the utmost common form of dementia among the geriatric community. In the pathogenesis of AD, cerebrovascular dysfunction is revealed before the beginning of the cognitive decline. Mounting proof shows a precarious impact of cerebrovascular dysregulation in the development of AD pathology. Recent studies document that the mammalian target of rapamycin (mTOR) acts as a crucial effector of cerebrovascular dysregulation in AD. The mTOR contributes to brain vascular dysfunction and subsequence cerebral blood flow deficits as well as cognitive impairment. Furthermore, mTOR causes the blood–brain barrier (BBB) breakdown in AD models. Inhibition of mTOR hyperactivity protects the BBB integrity in AD. Furthermore, mTOR drives cognitive defect and cerebrovascular dysfunction, which are greatly prevalent in AD, but the central molecular mechanisms underlying these alterations are obscure. This review represents the crucial and current research findings regarding the role of mTOR signaling in cognitive aging and cerebrovascular dysfunction in the pathogenesis of AD. |
| doi_str_mv | 10.1002/iub.2324 |
| format | Article |
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Sahab ; Rahman, Md. Ataur ; Kabir, Md. Tanvir ; Behl, Tapan ; Mathew, Bijo ; Perveen, Asma ; Barreto, George E. ; Bin‐Jumah, May N. ; Abdel‐Daim, Mohamed M. ; Ashraf, Ghulam Md</creator><creatorcontrib>Uddin, Md. Sahab ; Rahman, Md. Ataur ; Kabir, Md. Tanvir ; Behl, Tapan ; Mathew, Bijo ; Perveen, Asma ; Barreto, George E. ; Bin‐Jumah, May N. ; Abdel‐Daim, Mohamed M. ; Ashraf, Ghulam Md</creatorcontrib><description>Age‐related cognitive failure is a main devastating incident affecting even healthy people. Alzheimer's disease (AD) is the utmost common form of dementia among the geriatric community. In the pathogenesis of AD, cerebrovascular dysfunction is revealed before the beginning of the cognitive decline. Mounting proof shows a precarious impact of cerebrovascular dysregulation in the development of AD pathology. Recent studies document that the mammalian target of rapamycin (mTOR) acts as a crucial effector of cerebrovascular dysregulation in AD. The mTOR contributes to brain vascular dysfunction and subsequence cerebral blood flow deficits as well as cognitive impairment. Furthermore, mTOR causes the blood–brain barrier (BBB) breakdown in AD models. Inhibition of mTOR hyperactivity protects the BBB integrity in AD. Furthermore, mTOR drives cognitive defect and cerebrovascular dysfunction, which are greatly prevalent in AD, but the central molecular mechanisms underlying these alterations are obscure. This review represents the crucial and current research findings regarding the role of mTOR signaling in cognitive aging and cerebrovascular dysfunction in the pathogenesis of AD.</description><identifier>ISSN: 1521-6543</identifier><identifier>EISSN: 1521-6551</identifier><identifier>DOI: 10.1002/iub.2324</identifier><identifier>PMID: 32472959</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>Aging ; Alzheimer's disease ; Biochemistry & Molecular Biology ; Blood flow ; Blood-brain barrier ; Cell Biology ; Cerebral blood flow ; cerebrovascular dysfunction ; Cognitive ability ; cognitive aging ; Dementia disorders ; Hyperactivity ; Life Sciences & Biomedicine ; Molecular modelling ; mTOR ; Neurodegenerative diseases ; Pathogenesis ; Rapamycin ; Science & Technology ; TOR protein</subject><ispartof>IUBMB life, 2020-09, Vol.72 (9), p.1843-1855</ispartof><rights>2020 International Union of Biochemistry and Molecular Biology</rights><rights>2020 International Union of Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>46</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000536299100001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c3834-ac0b4be2034000439af4f7cb49d0e488ac59d4af89de922337df5459bd02796c3</citedby><cites>FETCH-LOGICAL-c3834-ac0b4be2034000439af4f7cb49d0e488ac59d4af89de922337df5459bd02796c3</cites><orcidid>0000-0002-6644-1971 ; 0000-0002-0805-7840 ; 0000-0001-6649-3694 ; 0000-0002-4341-2713 ; 0000-0002-6078-8587 ; 0000-0002-3017-9924</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fiub.2324$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fiub.2324$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,1434,27929,27930,28253,45579,45580,46414,46838</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32472959$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Uddin, Md. 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| subjects | Aging Alzheimer's disease Biochemistry & Molecular Biology Blood flow Blood-brain barrier Cell Biology Cerebral blood flow cerebrovascular dysfunction Cognitive ability cognitive aging Dementia disorders Hyperactivity Life Sciences & Biomedicine Molecular modelling mTOR Neurodegenerative diseases Pathogenesis Rapamycin Science & Technology TOR protein |
| title | Multifarious roles of mTOR signaling in cognitive aging and cerebrovascular dysfunction of Alzheimer's disease |
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