Antiseizure Medications in Alzheimer’s Disease from Preclinical to Clinical Evidence
Alzheimer’s disease (AD) and epilepsy are common neurological disorders in the elderly. A bi-directional link between these neurological diseases has been reported, with patients with either condition carrying almost a two-fold risk of contracting the other compared to healthy subjects. AD/epilepsy...
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Veröffentlicht in: | International journal of molecular sciences 2023-08, Vol.24 (16), p.12639 |
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description | Alzheimer’s disease (AD) and epilepsy are common neurological disorders in the elderly. A bi-directional link between these neurological diseases has been reported, with patients with either condition carrying almost a two-fold risk of contracting the other compared to healthy subjects. AD/epilepsy adversely affects patients’ quality of life and represents a severe public health problem. Thus, identifying the relationship between epilepsy and AD represents an ongoing challenge and continuing need. Seizures in AD patients are often unrecognized because they are often nonconvulsive and sometimes mimic some behavioral symptoms of AD. Regarding this, it has been hypothesized that epileptogenesis and neurodegeneration share common underlying mechanisms. Targeted treatment to decrease epileptiform activity could represent a valuable strategy for delaying the neurodegenerative process and related cognitive impairment. Several preclinical studies have shown that some antiseizure medications (ASMs) targeting abnormal network hyperexcitability may change the natural progression of AD. However, to date, no guidelines are available for managing seizures in AD patients because of the paucity of randomized clinical trials sufficient for answering the correlated questions. Future AD clinical studies are mandatory to update clinicians about the symptomatic treatment of seizures in AD patients and recognize whether ASM therapy could change the natural progression of the disease, thereby rescuing cognitive performance. |
doi_str_mv | 10.3390/ijms241612639 |
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A bi-directional link between these neurological diseases has been reported, with patients with either condition carrying almost a two-fold risk of contracting the other compared to healthy subjects. AD/epilepsy adversely affects patients’ quality of life and represents a severe public health problem. Thus, identifying the relationship between epilepsy and AD represents an ongoing challenge and continuing need. Seizures in AD patients are often unrecognized because they are often nonconvulsive and sometimes mimic some behavioral symptoms of AD. Regarding this, it has been hypothesized that epileptogenesis and neurodegeneration share common underlying mechanisms. Targeted treatment to decrease epileptiform activity could represent a valuable strategy for delaying the neurodegenerative process and related cognitive impairment. Several preclinical studies have shown that some antiseizure medications (ASMs) targeting abnormal network hyperexcitability may change the natural progression of AD. However, to date, no guidelines are available for managing seizures in AD patients because of the paucity of randomized clinical trials sufficient for answering the correlated questions. Future AD clinical studies are mandatory to update clinicians about the symptomatic treatment of seizures in AD patients and recognize whether ASM therapy could change the natural progression of the disease, thereby rescuing cognitive performance.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms241612639</identifier><identifier>PMID: 37628821</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Advertising executives ; Alzheimer's disease ; Anticonvulsants ; Cognitive ability ; Comorbidity ; Comparative analysis ; Convulsions & seizures ; Dementia ; Development and progression ; Drug therapy ; Drugs ; Epilepsy ; Kinases ; Medical research ; Medicine, Experimental ; Neurodegeneration ; Pathogenesis ; Proteins ; Review ; Seizures (Medicine) ; Transgenic animals ; Type 2 diabetes</subject><ispartof>International journal of molecular sciences, 2023-08, Vol.24 (16), p.12639</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/). 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A bi-directional link between these neurological diseases has been reported, with patients with either condition carrying almost a two-fold risk of contracting the other compared to healthy subjects. AD/epilepsy adversely affects patients’ quality of life and represents a severe public health problem. Thus, identifying the relationship between epilepsy and AD represents an ongoing challenge and continuing need. Seizures in AD patients are often unrecognized because they are often nonconvulsive and sometimes mimic some behavioral symptoms of AD. Regarding this, it has been hypothesized that epileptogenesis and neurodegeneration share common underlying mechanisms. Targeted treatment to decrease epileptiform activity could represent a valuable strategy for delaying the neurodegenerative process and related cognitive impairment. Several preclinical studies have shown that some antiseizure medications (ASMs) targeting abnormal network hyperexcitability may change the natural progression of AD. However, to date, no guidelines are available for managing seizures in AD patients because of the paucity of randomized clinical trials sufficient for answering the correlated questions. Future AD clinical studies are mandatory to update clinicians about the symptomatic treatment of seizures in AD patients and recognize whether ASM therapy could change the natural progression of the disease, thereby rescuing cognitive performance.</description><subject>Advertising executives</subject><subject>Alzheimer's disease</subject><subject>Anticonvulsants</subject><subject>Cognitive ability</subject><subject>Comorbidity</subject><subject>Comparative analysis</subject><subject>Convulsions & seizures</subject><subject>Dementia</subject><subject>Development and progression</subject><subject>Drug therapy</subject><subject>Drugs</subject><subject>Epilepsy</subject><subject>Kinases</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Neurodegeneration</subject><subject>Pathogenesis</subject><subject>Proteins</subject><subject>Review</subject><subject>Seizures (Medicine)</subject><subject>Transgenic animals</subject><subject>Type 2 diabetes</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>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkstO3DAUhq2qqMOly-4jddNNwNfEXlWjYaCVQLAAtpZxjgePEpvaCVJn1dfg9XgSMtzEVMgLHx1__3_0WwehbwTvM6bwgV92mXJSEVox9QltE05piXFVf35XT9BOzkuMKaNCfUETVldUSkq20dU09D6DXw0JilNovDW9jyEXPhTTdnUDvoP08O8-F4cjZjIULsWuOE9gWx9Gui36WMxe6_mdbyBY2ENbzrQZvr7cu-jyaH4x-1WenB3_nk1PSssr3JeVawS1jBrHHVESHEDTEOVqAGeIlPxaMkUxJ4ICWEysaGpHmaiUIGst20U_n31vh-sOGguhT6bVt8l3Jv3V0Xi9-RL8jV7EO00wF1yxtcOPF4cU_wyQe935bKFtTYA4ZE2lqCXn9RP6_T90GYcUxnxPFJZM1O-ohWlB--DiONiuTfV0_HZeK0zxSO1_QI2ngc7bGMD5sb8hKJ8FNsWcE7i3kATr9SbojU1gjxLKpZ8</recordid><startdate>20230801</startdate><enddate>20230801</enddate><creator>Bosco, Francesca</creator><creator>Guarnieri, Lorenza</creator><creator>Rania, Vincenzo</creator><creator>Palma, Ernesto</creator><creator>Citraro, Rita</creator><creator>Corasaniti, Maria Tiziana</creator><creator>Leo, Antonio</creator><creator>De Sarro, Giovambattista</creator><general>MDPI AG</general><general>MDPI</general><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/0000-0002-0061-1608</orcidid><orcidid>https://orcid.org/0000-0003-4199-207X</orcidid><orcidid>https://orcid.org/0000-0002-7629-6579</orcidid><orcidid>https://orcid.org/0000-0001-6746-6751</orcidid><orcidid>https://orcid.org/0000-0001-6472-0697</orcidid><orcidid>https://orcid.org/0009-0004-4766-9710</orcidid></search><sort><creationdate>20230801</creationdate><title>Antiseizure Medications in Alzheimer’s Disease from Preclinical to Clinical Evidence</title><author>Bosco, Francesca ; 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A bi-directional link between these neurological diseases has been reported, with patients with either condition carrying almost a two-fold risk of contracting the other compared to healthy subjects. AD/epilepsy adversely affects patients’ quality of life and represents a severe public health problem. Thus, identifying the relationship between epilepsy and AD represents an ongoing challenge and continuing need. Seizures in AD patients are often unrecognized because they are often nonconvulsive and sometimes mimic some behavioral symptoms of AD. Regarding this, it has been hypothesized that epileptogenesis and neurodegeneration share common underlying mechanisms. Targeted treatment to decrease epileptiform activity could represent a valuable strategy for delaying the neurodegenerative process and related cognitive impairment. Several preclinical studies have shown that some antiseizure medications (ASMs) targeting abnormal network hyperexcitability may change the natural progression of AD. However, to date, no guidelines are available for managing seizures in AD patients because of the paucity of randomized clinical trials sufficient for answering the correlated questions. Future AD clinical studies are mandatory to update clinicians about the symptomatic treatment of seizures in AD patients and recognize whether ASM therapy could change the natural progression of the disease, thereby rescuing cognitive performance.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>37628821</pmid><doi>10.3390/ijms241612639</doi><orcidid>https://orcid.org/0000-0002-0061-1608</orcidid><orcidid>https://orcid.org/0000-0003-4199-207X</orcidid><orcidid>https://orcid.org/0000-0002-7629-6579</orcidid><orcidid>https://orcid.org/0000-0001-6746-6751</orcidid><orcidid>https://orcid.org/0000-0001-6472-0697</orcidid><orcidid>https://orcid.org/0009-0004-4766-9710</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Advertising executives Alzheimer's disease Anticonvulsants Cognitive ability Comorbidity Comparative analysis Convulsions & seizures Dementia Development and progression Drug therapy Drugs Epilepsy Kinases Medical research Medicine, Experimental Neurodegeneration Pathogenesis Proteins Review Seizures (Medicine) Transgenic animals Type 2 diabetes |
title | Antiseizure Medications in Alzheimer’s Disease from Preclinical to Clinical Evidence |
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