Aβ1-42 Accumulation Accompanies Changed Expression of Ly6/uPAR Proteins, Dysregulation of the Cholinergic System, and Degeneration of Astrocytes in the Cerebellum of Mouse Model of Early Alzheimer Disease
Alzheimer disease (AD) is a widespread neurodegenerative disease characterized by the accumulation of oligomeric toxic forms of β-amyloid (Aβ1-42) and dysfunction of the cholinergic system in the different brain regions. However, the exact mechanisms of AD pathogenesis and the role of the nicotinic...
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| Veröffentlicht in: | International journal of molecular sciences 2023-10, Vol.24 (19), p.14852 |
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| creator | Bychkov, Maxim L Isaev, Aizek B Andreev-Andrievskiy, Alexander A Petrov, Konstantin Paramonov, Alexander S Kirpichnikov, Mikhail P Lyukmanova, Ekaterina N |
| description | Alzheimer disease (AD) is a widespread neurodegenerative disease characterized by the accumulation of oligomeric toxic forms of β-amyloid (Aβ1-42) and dysfunction of the cholinergic system in the different brain regions. However, the exact mechanisms of AD pathogenesis and the role of the nicotinic acetylcholine receptors (nAChRs) in the disease progression remain unclear. Here, we revealed a decreased expression of a number of the Ly6/uPAR proteins targeting nAChRs in the cerebellum of 2xTg-AD mice (model of early AD) in comparison with non-transgenic mice both at mRNA and protein levels. We showed that co-localization of one of them, - neuromodulator Lynx1, with α7-nAChR was diminished in the vicinity of cerebellar astrocytes of 2xTg-AD mice, while Aβ1-42 co-localization with this receptor present was increased. Moreover, the expression of anti-inflammatory transcription factor KLF4 regulating transcription of the
genes was decreased in the cerebellum of 2xTg-AD mice, while expression of inflammatory cytokine TNF-α was increased. Based on these data together with observed astrocyte degeneration in the cerebellum of 2xTg-AD mice, we suggest the mechanism by which expression of the Ly6/uPAR proteins upon Aβ pathology results in dysregulation of the cholinergic system and particularly of α7-nAChR function in the cerebellum. This leads to enhanced neuroinflammation and cerebellar astrocyte degeneration. |
| doi_str_mv | 10.3390/ijms241914852 |
| format | Article |
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genes was decreased in the cerebellum of 2xTg-AD mice, while expression of inflammatory cytokine TNF-α was increased. Based on these data together with observed astrocyte degeneration in the cerebellum of 2xTg-AD mice, we suggest the mechanism by which expression of the Ly6/uPAR proteins upon Aβ pathology results in dysregulation of the cholinergic system and particularly of α7-nAChR function in the cerebellum. This leads to enhanced neuroinflammation and cerebellar astrocyte degeneration.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms241914852</identifier><identifier>PMID: 37834299</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Advertising executives ; alpha7 Nicotinic Acetylcholine Receptor - genetics ; alpha7 Nicotinic Acetylcholine Receptor - metabolism ; Alzheimer Disease - metabolism ; Alzheimer's disease ; Amyloid beta-Peptides - metabolism ; Analysis ; Animals ; Astrocytes - metabolism ; Brain ; Cerebellum - metabolism ; Cholinergic Agents - metabolism ; Cognitive ability ; Genes ; Genetic engineering ; Genetic transcription ; Localization ; Mice ; Neurodegenerative Diseases - metabolism ; Peptides ; Physiological aspects ; Proteins ; Receptors, Nicotinic - metabolism ; RNA ; Target marketing ; Transcription factors ; Transgenic animals</subject><ispartof>International journal of molecular sciences, 2023-10, Vol.24 (19), p.14852</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-c66d9b1e9ea79a171453529aa29174ef7c59079cb89d5d8bf0fba8576dd2108b3</citedby><cites>FETCH-LOGICAL-c483t-c66d9b1e9ea79a171453529aa29174ef7c59079cb89d5d8bf0fba8576dd2108b3</cites><orcidid>0009-0007-9913-1842 ; 0000-0002-1173-8153</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10573428/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10573428/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37834299$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bychkov, Maxim L</creatorcontrib><creatorcontrib>Isaev, Aizek B</creatorcontrib><creatorcontrib>Andreev-Andrievskiy, Alexander A</creatorcontrib><creatorcontrib>Petrov, Konstantin</creatorcontrib><creatorcontrib>Paramonov, Alexander S</creatorcontrib><creatorcontrib>Kirpichnikov, Mikhail P</creatorcontrib><creatorcontrib>Lyukmanova, Ekaterina N</creatorcontrib><title>Aβ1-42 Accumulation Accompanies Changed Expression of Ly6/uPAR Proteins, Dysregulation of the Cholinergic System, and Degeneration of Astrocytes in the Cerebellum of Mouse Model of Early Alzheimer Disease</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Alzheimer disease (AD) is a widespread neurodegenerative disease characterized by the accumulation of oligomeric toxic forms of β-amyloid (Aβ1-42) and dysfunction of the cholinergic system in the different brain regions. However, the exact mechanisms of AD pathogenesis and the role of the nicotinic acetylcholine receptors (nAChRs) in the disease progression remain unclear. Here, we revealed a decreased expression of a number of the Ly6/uPAR proteins targeting nAChRs in the cerebellum of 2xTg-AD mice (model of early AD) in comparison with non-transgenic mice both at mRNA and protein levels. We showed that co-localization of one of them, - neuromodulator Lynx1, with α7-nAChR was diminished in the vicinity of cerebellar astrocytes of 2xTg-AD mice, while Aβ1-42 co-localization with this receptor present was increased. Moreover, the expression of anti-inflammatory transcription factor KLF4 regulating transcription of the
genes was decreased in the cerebellum of 2xTg-AD mice, while expression of inflammatory cytokine TNF-α was increased. Based on these data together with observed astrocyte degeneration in the cerebellum of 2xTg-AD mice, we suggest the mechanism by which expression of the Ly6/uPAR proteins upon Aβ pathology results in dysregulation of the cholinergic system and particularly of α7-nAChR function in the cerebellum. This leads to enhanced neuroinflammation and cerebellar astrocyte degeneration.</description><subject>Advertising executives</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - genetics</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Analysis</subject><subject>Animals</subject><subject>Astrocytes - metabolism</subject><subject>Brain</subject><subject>Cerebellum - metabolism</subject><subject>Cholinergic Agents - metabolism</subject><subject>Cognitive ability</subject><subject>Genes</subject><subject>Genetic engineering</subject><subject>Genetic transcription</subject><subject>Localization</subject><subject>Mice</subject><subject>Neurodegenerative Diseases - metabolism</subject><subject>Peptides</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Receptors, Nicotinic - metabolism</subject><subject>RNA</subject><subject>Target marketing</subject><subject>Transcription factors</subject><subject>Transgenic animals</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkktv1DAQxyMEoqVw5IoiceHQtH4kcXxC0e7ykBZR8ThbjjPJepXYWztBpB-r3wM-E462XboIWbI9nt_8RzOeKHqJ0QWlHF3qbe9JijlOi4w8ik5xSkiCUM4eP7ifRM-83yJEKMn40-iEsoKmhPPT6Ff5-xYnKYlLpcZ-7OSgrZkN2--k0eDjxUaaFup49XPnwPvZbZt4PeWX41X5Jb5ydgBt_Hm8nLyD9l4iMMMGQrTttAHXahV_nfwA_XksTR0voYXwfGBLPzirpiEk1GYfCQ4q6Lqxn_2f7Ogh7DV0s7mSrpvisrvZgO7BxUvtQXp4Hj1pZOfhxd15Fn1_t_q2-JCsP7__uCjXiUoLOiQqz2teYeAgGZeY4TSjGeFSEo5ZCg1TGUeMq6rgdVYXVYOaShYZy-uaYFRU9Cx6u9fdjVUPtQIzONmJndO9dJOwUotjj9Eb0dofAqOMhc4XQeHNnYKz1yP4QfTaq1CuNBBKFaRgjHKCMQno63_QrR2dCfXNVB4wzPO_VCs7ENo0NiRWs6goGQvzgQijgbr4DxVWDb1W1kCjw_tRQLIPUM768L_NoUiMxDyA4mgAA__qYWcO9P3E0T9C_tkd</recordid><startdate>20231001</startdate><enddate>20231001</enddate><creator>Bychkov, Maxim L</creator><creator>Isaev, Aizek B</creator><creator>Andreev-Andrievskiy, Alexander A</creator><creator>Petrov, Konstantin</creator><creator>Paramonov, Alexander S</creator><creator>Kirpichnikov, Mikhail P</creator><creator>Lyukmanova, Ekaterina N</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0009-0007-9913-1842</orcidid><orcidid>https://orcid.org/0000-0002-1173-8153</orcidid></search><sort><creationdate>20231001</creationdate><title>Aβ1-42 Accumulation Accompanies Changed Expression of Ly6/uPAR Proteins, Dysregulation of the Cholinergic System, and Degeneration of Astrocytes in the Cerebellum of Mouse Model of Early Alzheimer Disease</title><author>Bychkov, Maxim L ; 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However, the exact mechanisms of AD pathogenesis and the role of the nicotinic acetylcholine receptors (nAChRs) in the disease progression remain unclear. Here, we revealed a decreased expression of a number of the Ly6/uPAR proteins targeting nAChRs in the cerebellum of 2xTg-AD mice (model of early AD) in comparison with non-transgenic mice both at mRNA and protein levels. We showed that co-localization of one of them, - neuromodulator Lynx1, with α7-nAChR was diminished in the vicinity of cerebellar astrocytes of 2xTg-AD mice, while Aβ1-42 co-localization with this receptor present was increased. Moreover, the expression of anti-inflammatory transcription factor KLF4 regulating transcription of the
genes was decreased in the cerebellum of 2xTg-AD mice, while expression of inflammatory cytokine TNF-α was increased. Based on these data together with observed astrocyte degeneration in the cerebellum of 2xTg-AD mice, we suggest the mechanism by which expression of the Ly6/uPAR proteins upon Aβ pathology results in dysregulation of the cholinergic system and particularly of α7-nAChR function in the cerebellum. This leads to enhanced neuroinflammation and cerebellar astrocyte degeneration.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37834299</pmid><doi>10.3390/ijms241914852</doi><orcidid>https://orcid.org/0009-0007-9913-1842</orcidid><orcidid>https://orcid.org/0000-0002-1173-8153</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Advertising executives alpha7 Nicotinic Acetylcholine Receptor - genetics alpha7 Nicotinic Acetylcholine Receptor - metabolism Alzheimer Disease - metabolism Alzheimer's disease Amyloid beta-Peptides - metabolism Analysis Animals Astrocytes - metabolism Brain Cerebellum - metabolism Cholinergic Agents - metabolism Cognitive ability Genes Genetic engineering Genetic transcription Localization Mice Neurodegenerative Diseases - metabolism Peptides Physiological aspects Proteins Receptors, Nicotinic - metabolism RNA Target marketing Transcription factors Transgenic animals |
| title | Aβ1-42 Accumulation Accompanies Changed Expression of Ly6/uPAR Proteins, Dysregulation of the Cholinergic System, and Degeneration of Astrocytes in the Cerebellum of Mouse Model of Early Alzheimer Disease |
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