Limitations and potential strategies of immune checkpoint blockade in age-related neurodegenerative disorders
Neurological disorders such as Alzheimer's disease (AD), and Parkinson's disease (PD) have no disease-modifying treatments, resulting in a global dementia crisis that affects more than 50 million people. Amyloid-beta (Aβ), tau, and alpha-synuclein (α-Syn) are three crucial proteins that ar...
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| Veröffentlicht in: | The journal of physiological sciences 2024-09, Vol.74 (1), p.46, Article 46 |
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| creator | Lasheen, Noha N Allam, Salma Elgarawany, Abdullrahman Aswa, Darin W Mansour, Rana Farouk, Ziad |
| description | Neurological disorders such as Alzheimer's disease (AD), and Parkinson's disease (PD) have no disease-modifying treatments, resulting in a global dementia crisis that affects more than 50 million people. Amyloid-beta (Aβ), tau, and alpha-synuclein (α-Syn) are three crucial proteins that are involved in the pathogenesis of these age-related neurodegenerative diseases. Only a few approved AD medications have been used in the clinic up to this point, and their results are only partial symptomatic alleviation for AD patients and cannot stop the progression of AD. Immunotherapies have attracted considerable interest as they target certain protein strains and conformations as well as promote clearance. Immunotherapies also have the potential to be neuroprotective: as they limit synaptic damage and spread of neuroinflammation by neutralizing extracellular protein aggregates. Lately, disease-modifying therapies (DMTs) that can alter the pathophysiology that underlies AD with anti-Aβ monoclonal antibodies (MAbs) (e.g., aducanumab, lecanemab, gantenerumab, donanemab, solanezumab, crenezumab, tilavonemab). Similarly, in Parkinson's disease (PD), DMTs utilizing anti-αSyn (MAbs) (e.g., prasinezumab, cinpanemab,) are progressively being developed and evaluated in clinical trials. These therapies are based on the hypothesis that both AD and PD may involve systemic impairments in cell-dependent clearance mechanisms of amyloid-beta (Aβ) and alpha-synuclein (αSyn), respectively, meaning the body's overall inability to effectively remove Aβ and αSyn due to malfunctioning cellular mechanisms. In this review we will provide possible evidence behind the use of immunotherapy with MAbs in AD and PD and highlight the recent clinical development landscape of anti-Aβ (MAbs) and anti-αSyn (MAbs) from these clinical trials in order to better investigate the therapeutic possibilities and adverse effects of these anti-Aβ and anti-αSyn MAbs on AD and PD. |
| doi_str_mv | 10.1186/s12576-024-00933-4 |
| format | Article |
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Amyloid-beta (Aβ), tau, and alpha-synuclein (α-Syn) are three crucial proteins that are involved in the pathogenesis of these age-related neurodegenerative diseases. Only a few approved AD medications have been used in the clinic up to this point, and their results are only partial symptomatic alleviation for AD patients and cannot stop the progression of AD. Immunotherapies have attracted considerable interest as they target certain protein strains and conformations as well as promote clearance. Immunotherapies also have the potential to be neuroprotective: as they limit synaptic damage and spread of neuroinflammation by neutralizing extracellular protein aggregates. Lately, disease-modifying therapies (DMTs) that can alter the pathophysiology that underlies AD with anti-Aβ monoclonal antibodies (MAbs) (e.g., aducanumab, lecanemab, gantenerumab, donanemab, solanezumab, crenezumab, tilavonemab). Similarly, in Parkinson's disease (PD), DMTs utilizing anti-αSyn (MAbs) (e.g., prasinezumab, cinpanemab,) are progressively being developed and evaluated in clinical trials. These therapies are based on the hypothesis that both AD and PD may involve systemic impairments in cell-dependent clearance mechanisms of amyloid-beta (Aβ) and alpha-synuclein (αSyn), respectively, meaning the body's overall inability to effectively remove Aβ and αSyn due to malfunctioning cellular mechanisms. In this review we will provide possible evidence behind the use of immunotherapy with MAbs in AD and PD and highlight the recent clinical development landscape of anti-Aβ (MAbs) and anti-αSyn (MAbs) from these clinical trials in order to better investigate the therapeutic possibilities and adverse effects of these anti-Aβ and anti-αSyn MAbs on AD and PD.</description><identifier>ISSN: 1880-6562</identifier><identifier>ISSN: 1880-6546</identifier><identifier>EISSN: 1880-6562</identifier><identifier>DOI: 10.1186/s12576-024-00933-4</identifier><identifier>PMID: 39313800</identifier><language>eng</language><publisher>Japan: Springer</publisher><subject>Advertising executives ; Aging - immunology ; alpha-Synuclein - antagonists & inhibitors ; alpha-Synuclein - immunology ; alpha-Synuclein - metabolism ; Alzheimer Disease - drug therapy ; Alzheimer Disease - immunology ; Alzheimer Disease - metabolism ; Alzheimer's disease ; Amyloid beta-Peptides - immunology ; Amyloid beta-Peptides - metabolism ; Animals ; B cells ; Development and progression ; Health aspects ; Humans ; Immune Checkpoint Inhibitors - pharmacology ; Immune Checkpoint Inhibitors - therapeutic use ; Immunotherapy ; Immunotherapy - methods ; Medical research ; Medicine, Experimental ; Monoclonal antibodies ; Nervous system diseases ; Neurodegenerative Diseases - drug therapy ; Neurodegenerative Diseases - immunology ; Neurophysiology ; Parkinson Disease - drug therapy ; Parkinson Disease - immunology ; Parkinson Disease - therapy ; Proteins ; Review</subject><ispartof>The journal of physiological sciences, 2024-09, Vol.74 (1), p.46, Article 46</ispartof><rights>2024. The Author(s).</rights><rights>COPYRIGHT 2024 Springer</rights><rights>The Author(s) 2024 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c312t-7fabc19d35361c25a66d40bd5d204ed09b243ed71e2ec7f371512050cdcd5cbe3</cites><orcidid>0009-0003-6402-0625 ; 0009-0004-1124-8084 ; 0009-0007-0717-9225 ; 0000-0002-5418-2191 ; 0009-0005-2749-8982 ; 0009-0003-8820-5480</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/PMC11421184/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11421184/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39313800$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lasheen, Noha N</creatorcontrib><creatorcontrib>Allam, Salma</creatorcontrib><creatorcontrib>Elgarawany, Abdullrahman</creatorcontrib><creatorcontrib>Aswa, Darin W</creatorcontrib><creatorcontrib>Mansour, Rana</creatorcontrib><creatorcontrib>Farouk, Ziad</creatorcontrib><title>Limitations and potential strategies of immune checkpoint blockade in age-related neurodegenerative disorders</title><title>The journal of physiological sciences</title><addtitle>J Physiol Sci</addtitle><description>Neurological disorders such as Alzheimer's disease (AD), and Parkinson's disease (PD) have no disease-modifying treatments, resulting in a global dementia crisis that affects more than 50 million people. Amyloid-beta (Aβ), tau, and alpha-synuclein (α-Syn) are three crucial proteins that are involved in the pathogenesis of these age-related neurodegenerative diseases. Only a few approved AD medications have been used in the clinic up to this point, and their results are only partial symptomatic alleviation for AD patients and cannot stop the progression of AD. Immunotherapies have attracted considerable interest as they target certain protein strains and conformations as well as promote clearance. Immunotherapies also have the potential to be neuroprotective: as they limit synaptic damage and spread of neuroinflammation by neutralizing extracellular protein aggregates. Lately, disease-modifying therapies (DMTs) that can alter the pathophysiology that underlies AD with anti-Aβ monoclonal antibodies (MAbs) (e.g., aducanumab, lecanemab, gantenerumab, donanemab, solanezumab, crenezumab, tilavonemab). Similarly, in Parkinson's disease (PD), DMTs utilizing anti-αSyn (MAbs) (e.g., prasinezumab, cinpanemab,) are progressively being developed and evaluated in clinical trials. These therapies are based on the hypothesis that both AD and PD may involve systemic impairments in cell-dependent clearance mechanisms of amyloid-beta (Aβ) and alpha-synuclein (αSyn), respectively, meaning the body's overall inability to effectively remove Aβ and αSyn due to malfunctioning cellular mechanisms. In this review we will provide possible evidence behind the use of immunotherapy with MAbs in AD and PD and highlight the recent clinical development landscape of anti-Aβ (MAbs) and anti-αSyn (MAbs) from these clinical trials in order to better investigate the therapeutic possibilities and adverse effects of these anti-Aβ and anti-αSyn MAbs on AD and PD.</description><subject>Advertising executives</subject><subject>Aging - immunology</subject><subject>alpha-Synuclein - antagonists & inhibitors</subject><subject>alpha-Synuclein - immunology</subject><subject>alpha-Synuclein - metabolism</subject><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - immunology</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - immunology</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animals</subject><subject>B cells</subject><subject>Development and progression</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Immune Checkpoint Inhibitors - pharmacology</subject><subject>Immune Checkpoint Inhibitors - therapeutic use</subject><subject>Immunotherapy</subject><subject>Immunotherapy - methods</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Monoclonal antibodies</subject><subject>Nervous system diseases</subject><subject>Neurodegenerative Diseases - drug therapy</subject><subject>Neurodegenerative Diseases - immunology</subject><subject>Neurophysiology</subject><subject>Parkinson Disease - drug therapy</subject><subject>Parkinson Disease - immunology</subject><subject>Parkinson Disease - therapy</subject><subject>Proteins</subject><subject>Review</subject><issn>1880-6562</issn><issn>1880-6546</issn><issn>1880-6562</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1u1TAQRi1ERUvhBVggS2zYhHrs2ElWqKr4k67Epl1bjj1JTRP7YjuV-vb4cktVVmNpjo9m5iPkHbBPAL26yMBlpxrG24axQYimfUHOoO9Zo6TiL5-9T8nrnH8x1qqB96_IqRgEiJ6xM7Lu_OqLKT6GTE1wdB8LhuLNQnNJpuDsMdM4Ub-uW0Bqb9He7aMPhY5LtHfGIfWBmhmbhEvlHQ24pehwxoBV4O-ROp9jcpjyG3IymSXj28d6Tm6-frm--t7sfn77cXW5a6wAXppuMqOFwQkpFFgujVKuZaOTjrMWHRtG3gp0HSBH202iAwmcSWadddKOKM7J56N3v40rOls3SmbR--RXkx50NF7_3wn-Vs_xXgO0vN62rYaPj4YUf2-Yi159trgsJmDcshbA-k6JetyKfjiis1lQ-zDFqrQHXF_2bOgApDpQ_EjZFHNOOD1NA0wf4tTHOHWNU_-NUx-meP98j6cv__ITfwBoeJ4I</recordid><startdate>20240923</startdate><enddate>20240923</enddate><creator>Lasheen, Noha N</creator><creator>Allam, Salma</creator><creator>Elgarawany, Abdullrahman</creator><creator>Aswa, Darin W</creator><creator>Mansour, Rana</creator><creator>Farouk, Ziad</creator><general>Springer</general><general>BioMed Central</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0009-0003-6402-0625</orcidid><orcidid>https://orcid.org/0009-0004-1124-8084</orcidid><orcidid>https://orcid.org/0009-0007-0717-9225</orcidid><orcidid>https://orcid.org/0000-0002-5418-2191</orcidid><orcidid>https://orcid.org/0009-0005-2749-8982</orcidid><orcidid>https://orcid.org/0009-0003-8820-5480</orcidid></search><sort><creationdate>20240923</creationdate><title>Limitations and potential strategies of immune checkpoint blockade in age-related neurodegenerative disorders</title><author>Lasheen, Noha N ; 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Amyloid-beta (Aβ), tau, and alpha-synuclein (α-Syn) are three crucial proteins that are involved in the pathogenesis of these age-related neurodegenerative diseases. Only a few approved AD medications have been used in the clinic up to this point, and their results are only partial symptomatic alleviation for AD patients and cannot stop the progression of AD. Immunotherapies have attracted considerable interest as they target certain protein strains and conformations as well as promote clearance. Immunotherapies also have the potential to be neuroprotective: as they limit synaptic damage and spread of neuroinflammation by neutralizing extracellular protein aggregates. Lately, disease-modifying therapies (DMTs) that can alter the pathophysiology that underlies AD with anti-Aβ monoclonal antibodies (MAbs) (e.g., aducanumab, lecanemab, gantenerumab, donanemab, solanezumab, crenezumab, tilavonemab). Similarly, in Parkinson's disease (PD), DMTs utilizing anti-αSyn (MAbs) (e.g., prasinezumab, cinpanemab,) are progressively being developed and evaluated in clinical trials. These therapies are based on the hypothesis that both AD and PD may involve systemic impairments in cell-dependent clearance mechanisms of amyloid-beta (Aβ) and alpha-synuclein (αSyn), respectively, meaning the body's overall inability to effectively remove Aβ and αSyn due to malfunctioning cellular mechanisms. In this review we will provide possible evidence behind the use of immunotherapy with MAbs in AD and PD and highlight the recent clinical development landscape of anti-Aβ (MAbs) and anti-αSyn (MAbs) from these clinical trials in order to better investigate the therapeutic possibilities and adverse effects of these anti-Aβ and anti-αSyn MAbs on AD and PD.</abstract><cop>Japan</cop><pub>Springer</pub><pmid>39313800</pmid><doi>10.1186/s12576-024-00933-4</doi><orcidid>https://orcid.org/0009-0003-6402-0625</orcidid><orcidid>https://orcid.org/0009-0004-1124-8084</orcidid><orcidid>https://orcid.org/0009-0007-0717-9225</orcidid><orcidid>https://orcid.org/0000-0002-5418-2191</orcidid><orcidid>https://orcid.org/0009-0005-2749-8982</orcidid><orcidid>https://orcid.org/0009-0003-8820-5480</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Advertising executives Aging - immunology alpha-Synuclein - antagonists & inhibitors alpha-Synuclein - immunology alpha-Synuclein - metabolism Alzheimer Disease - drug therapy Alzheimer Disease - immunology Alzheimer Disease - metabolism Alzheimer's disease Amyloid beta-Peptides - immunology Amyloid beta-Peptides - metabolism Animals B cells Development and progression Health aspects Humans Immune Checkpoint Inhibitors - pharmacology Immune Checkpoint Inhibitors - therapeutic use Immunotherapy Immunotherapy - methods Medical research Medicine, Experimental Monoclonal antibodies Nervous system diseases Neurodegenerative Diseases - drug therapy Neurodegenerative Diseases - immunology Neurophysiology Parkinson Disease - drug therapy Parkinson Disease - immunology Parkinson Disease - therapy Proteins Review |
| title | Limitations and potential strategies of immune checkpoint blockade in age-related neurodegenerative disorders |
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