Disease-Modifying Effects of Non-Invasive Electroceuticals on β-Amyloid Plaques and Tau Tangles for Alzheimer’s Disease

Abstract

Electroceuticals refer to various forms of electronic neurostimulators used for therapy. Interdisciplinary advances in medical engineering and science have led to the development of the electroceutical approach, which involves therapeutic agents that specifically target neural circuits, to realize precision therapy for Alzheimer’s disease (AD). To date, extensive studies have attempted to elucidate the disease-modifying effects of electroceuticals on areas in the brain of a patient with AD by the use of various physical stimuli, including electric, magnetic, and electromagnetic waves as well as ultrasound. Herein, we review non-invasive stimulatory systems and their effects on β-amyloid plaques and tau tangles, which are pathological molecular markers of AD. Therefore, this review will aid in better understanding the recent technological developments, applicable methods, and therapeutic effects of electronic stimulatory systems, including transcranial direct current stimulation, 40-Hz gamma oscillations, transcranial magnetic stimulation, electromagnetic field stimulation, infrared light stimulation and ionizing radiation therapy, and focused ultrasound for AD.

Charging Ahead: Examining the Future Therapeutic Potential of Electroceuticals

“…[21] At the molecular level, alternating electric field has been shown to degrade magnetite-bound protein aggregates in Alzheimer's disease via an electro-Fenton effect generated by electric-field-sensitized magnetite. [22,23] In another study, electrical stimulation (EStim) administered via gold nanoparticles functionalized with redox active molecules was shown to initiate quantum biological tunneling for electron transfer and triggered selective apoptosis of cancer cells. [24]…”

Posterity of nanoscience as lipid nanosystems for Alzheimer's disease regression

“…One of the main goals of AD treatment is to eliminate or prevent the production of these fragments of Aβ, as well as to improve the patient's survival, life quality, and function. Inhibition of the aggregation of Aβ, modification of the production of Aβ, immunotherapy focused against Aβ, and an increase in the degradation of Aβ are among the many therapeutics that target Aβ being studied [ 50 ]. Many treatments targeting Aβ peptides proved unsuccessful in clinical trials, and efforts to solve the problem are still underway.…”

The Role of Mitochondrial Dysfunction in Alzheimer’s: Molecular Defects and Mitophagy-Enhancing Approaches

“…Contrarily, the aggregation of Tau and Aβ42 generates mitochondrial impairment, modifies energy construction, and raises OS [45]. In addition, neurotoxic proteins also constrain glucose GLUT4 (transporter type 4) [48,49] and phosphofructokinase, delaying glucose intake, ATP synthesis, and aerobic glycolysis. These facts clearly indicate that the collaboration of these proteins is a source of neurodegenerative syndromes, supporting the assumption that mitochondrial impairment is an early instigator for AD [48], and creating an imperative to progress influential medications that relieve the bioenergetic shortfalls in susceptible nerve cells from the utmost AD-affected brain districts.…”