Felipe P Perez, Jorge Morisaki, Haitham Kanakri, Maher Rizkalla
Alzheimer's disease (AD) is the most common neurodegenerative dementia worldwide. AD is a multifactorial disease that causes a progressive decline in memory and function precipitated by toxic beta-amyloid (Aβ) proteins, a key player in AD pathology. In 2022, 6.5 million Americans lived with AD, costing the nation $321billion. The standard of care for AD treatment includes acetylcholinesterase inhibitors (AchEIs), NMDA receptor antagonists, and monoclonal antibodies (mAbs). However, these methods are either: 1) ineffective in improving cognition, 2) unable to change disease progression, 3) limited in the number of therapeutic targets, 4) prone to cause severe side effects (brain swelling, microhemorrhages with mAb, and bradycardia and syncope with AchEIs), 5) unable to effectively cross the blood-brain barrier, and 6) lack of understanding of the aging process on the disease. mAbs are available to lower Aβ, but the difficulties of reducing the levels of the toxic Aβ proteins in the brain without triggering brain swelling or microhemorrhages associated with mAbs make the risk-benefit profile of mAbs unclear. A novel multitarget, effective, and safe non-invasive approach utilizing Repeated Electromagnetic Field Stimulation (REMFS) lowers Aβ levels in human neurons and memory areas, prevents neuronal death, stops disease progression, and improves memory without causing brain edema or bleeds in AD mice. This REMFS treatment has not been developed for humans because current EMF devices have poor penetration depth and inhomogeneous E-field distribution in the brain. Here, we discussed the biology of these effects in neurons and the design of optimal devices to treat AD.
{"title":"Electromagnetic Field Stimulation Therapy for Alzheimer's Disease.","authors":"Felipe P Perez, Jorge Morisaki, Haitham Kanakri, Maher Rizkalla","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the most common neurodegenerative dementia worldwide. AD is a multifactorial disease that causes a progressive decline in memory and function precipitated by toxic beta-amyloid (Aβ) proteins, a key player in AD pathology. In 2022, 6.5 million Americans lived with AD, costing the nation $321billion. The standard of care for AD treatment includes acetylcholinesterase inhibitors (AchEIs), NMDA receptor antagonists, and monoclonal antibodies (mAbs). However, these methods are either: 1) ineffective in improving cognition, 2) unable to change disease progression, 3) limited in the number of therapeutic targets, 4) prone to cause severe side effects (brain swelling, microhemorrhages with mAb, and bradycardia and syncope with AchEIs), 5) unable to effectively cross the blood-brain barrier, and 6) lack of understanding of the aging process on the disease. mAbs are available to lower Aβ, but the difficulties of reducing the levels of the toxic Aβ proteins in the brain without triggering brain swelling or microhemorrhages associated with mAbs make the risk-benefit profile of mAbs unclear. A novel multitarget, effective, and safe non-invasive approach utilizing Repeated Electromagnetic Field Stimulation (REMFS) lowers Aβ levels in human neurons and memory areas, prevents neuronal death, stops disease progression, and improves memory without causing brain edema or bleeds in AD mice. This REMFS treatment has not been developed for humans because current EMF devices have poor penetration depth and inhomogeneous E-field distribution in the brain. Here, we discussed the biology of these effects in neurons and the design of optimal devices to treat AD.</p>","PeriodicalId":74280,"journal":{"name":"Neurology (Chicago, Ill.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11064876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140862907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A Dagra, A Barpujari, S Z Bauer, B O Olowofela, S Mohamed, K McGrath, C Robinson, S Robicsek, A Snyder, B Lucke-Wold
Epigenetic changes have been linked to a host of disease states. Besides the physiological function of epigenetic changes in regulating cellular function, recent data indicates that key changes in epigenetic activity also play an important pathophysiologic role following neurotrauma specifically. Such manifestations occur through the activation or silencing of different genes. Histone methylation has emerged as a critical component of this process and can be selectively modulated after injury. Pre-clinical studies have resulted in key discoveries regarding specific methylation sites of interest. This focused review highlights some of these early findings and their relationship to clinical outcomes. These findings suggest areas of future investigation and discovery in the quest to develop ideal biomarkers and methods to utilize them in developing therapeutic interventions.
{"title":"Epigenetics of Neurotrauma.","authors":"A Dagra, A Barpujari, S Z Bauer, B O Olowofela, S Mohamed, K McGrath, C Robinson, S Robicsek, A Snyder, B Lucke-Wold","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Epigenetic changes have been linked to a host of disease states. Besides the physiological function of epigenetic changes in regulating cellular function, recent data indicates that key changes in epigenetic activity also play an important pathophysiologic role following neurotrauma specifically. Such manifestations occur through the activation or silencing of different genes. Histone methylation has emerged as a critical component of this process and can be selectively modulated after injury. Pre-clinical studies have resulted in key discoveries regarding specific methylation sites of interest. This focused review highlights some of these early findings and their relationship to clinical outcomes. These findings suggest areas of future investigation and discovery in the quest to develop ideal biomarkers and methods to utilize them in developing therapeutic interventions.</p>","PeriodicalId":74280,"journal":{"name":"Neurology (Chicago, Ill.)","volume":"2 2","pages":"42-47"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10361119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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