Alzheimer’s Pathogenesis and Treatment by Transcranial Pulse Stimulation

Christiyan Naydenov; Teodora Manolova; Ivan Mindov

doi:10.3889/oamjms.2023.11564

Authors

Christiyan Naydenov Department of Neurology and Psychiatry, Medical Faculty, Trakia University, Stara Zagora, Bulgaria https://orcid.org/0000-0001-6082-4376
Teodora Manolova Department of Neurology and Psychiatry, Medical Faculty, Trakia University, Stara Zagora, Bulgaria
Ivan Mindov Department of Neurology and Psychiatry, Medical Faculty, Trakia University, Stara Zagora, Bulgaria https://orcid.org/0000-0001-9048-7614

DOI:

https://doi.org/10.3889/oamjms.2023.11564

Keywords:

Ultrasound brain stimulation, Alzheimer’s novel treatment, TPS effects

Abstract

The article discusses the use of transcranial pulse stimulation (TPS), a treatment method that uses ultrasound to penetrate the brain up to 8 cm. The article aims to review published studies on the effects of TPS on Alzheimer’s disease and to link the mechanism of the treatment with the pathophysiology of the disease. The discussion highlights the pathological triad of senile plaques, neurofibrillary tangles, and granular degeneration that causes Alzheimer’s disease. Patients with diabetes mellitus are predisposed to degenerative diseases, and the overlap between Alzheimer’s disease and obesity may be explained by the use of streptozotocin, which generates reactive oxygen species leading to DNA damage and cell death. The accumulation of beta-amyloid in the brain, mitochondrial malfunction, decreased production of ATP, and energy insufficiency is also discussed. The article concludes that TPS is a potential treatment for Alzheimer’s disease and that it can boost the expression of growth factors, enhance the flow of blood to the brain, trigger the creation of novel blood vessels, and promote the regeneration of nerves.

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References

Yahata K, Kanno H, Ozawa H, Yamaya S, Tateda S, Ito K, et al. Low-energy extracorporeal shock wave therapy for promotion of vascular endothelial growth factor expression and angiogenesis and improvement of locomotor and sensory functions after spinal cord injury. J Neurosurg Spine. 2016;25(6):745-55. https://doi.org/10.3171/2014.8.JNS132562 PMid:25280090 DOI: https://doi.org/10.3171/2016.4.SPINE15923

Hatanaka K, Ito K, Shindo T, Kagaya Y, Ogata T, Eguchi K, et al. Molecular mechanisms of the angiogenic effects of low-energy shock wave therapy: Roles of mechanotransduction. Am J Physiol Cell Physiol. 2016;311(3):C378-85. https://doi.org/10.1152/ajpcell.00152.2016 PMid:27413171 DOI: https://doi.org/10.1152/ajpcell.00152.2016

Mariotto S, Cavalieri E, Amelio E, Ciampa AR, de Prati AC, Marlinghaus E, et al, Extracorporeal shock waves: From lithotripsy to anti-inflammatory action by NO production. Nitric Oxide. 2005;12(2):89-96. https://doi.org/10.1016/j.niox.2004.12.005 PMid:15740982 DOI: https://doi.org/10.1016/j.niox.2004.12.005

D’Agostino MC, Craig K, Tibalt E, Respizzi S. Shock wave as biological therapeutic tool: From mechanical stimulation to recovery and healing, through mechanotransduction. Int J Surg. 2015;24(Pt B):147-53. https://doi.org/10.1016/j.niox.2004.12.005 PMid:15740982 DOI: https://doi.org/10.1016/j.ijsu.2015.11.030

López-Marín LM, Rivera AL, Fernández F, Loske AM. Shock wave-induced permeabilization of mammalian cells. Phys Life Rev. 2018;26-27:1-38. https://doi.org/10.1016/j.plrev.2018.03.001 PMid:29685859 DOI: https://doi.org/10.1016/j.plrev.2018.03.001

Wang B, Ning H, Reed-Maldonado AB, Zhou J, Ruan Y, Zhou T, et al. Low-Intensity extracorporeal shock wave therapy enhances brain-derived neurotrophic factor expression through PERK/ATF4 signaling pathway. Int J Mol Sci. 2017;18(2):433. https://doi.org/10.3390/ijms18020433 PMid:28212323 DOI: https://doi.org/10.3390/ijms18020433

Kroner Z. The relationship between Alzheimer’s disease and diabetes: Type 3 diabetes? Altern Med Rev. 2009;14(4):373-9. PMid:20030463

De la Monte SM. Brain insulin resistance and deficiency as therapeutic targets in Alzheimer’s disease. Curr Alzheimer Res. 2012;9(1):35-66. https://doi.org/10.2174/156720512799015037 PMid:22329651 DOI: https://doi.org/10.2174/156720512799015037

De la Monte SM. Insulin resistance and Alzheimer’s disease. BMB Rep. 2009;42(8):475-81. https://doi.org/10.5483/bmbrep.2009.42.8.475 PMid:19712582 DOI: https://doi.org/10.5483/BMBRep.2009.42.8.475

Messier C, Teutenberg K. The role of insulin, insulin growth factor, and insulin-degrading enzyme in brain aging and Alzheimer’s disease. Neural Plast. 2005;12(4):311-28. https://doi.org/10.1155/NP.2005.311 PMid:16444902 DOI: https://doi.org/10.1155/NP.2005.311

Frisoni GB, Altomare D, Thal DR, Ribaldi F, van der Kant R, Ossenkoppele R, et al. The probabilistic model of Alzheimer disease: The amyloid hypothesis revised. Nat Rev Neurosci. 2022;23(1):53-66. https://doi.org/10.1038/s41583-021-00533-w PMid:34815562 DOI: https://doi.org/10.1038/s41583-021-00533-w

Jagust W. Imaging the evolution and pathophysiology of Alzheimer disease. Nat Rev Neurosci. 2018;19(11):687-700. https://doi.org/10.1038/s41583-018-0067-3 PMid:30266970 DOI: https://doi.org/10.1038/s41583-018-0067-3

Karran E, De Strooper B. The amyloid hypothesis in Alzheimer disease: New insights from new therapeutics. Nat Rev Drug Discov. 2022;21(4):306-18. https://doi.org/10.1038/s41573-022-00391-w PMid:35177833 DOI: https://doi.org/10.1038/s41573-022-00391-w

Su J, Cavaco-Paulo A. Effect of ultrasound on protein functionality. Ultrason Sonochem. 2021;76:105653. https://doi.org/10.1016/j.ultsonch.2021.105653 PMid:34198127 DOI: https://doi.org/10.1016/j.ultsonch.2021.105653

Suslick KS, Grinstaff MW, Kolbeck KJ, Wong M. Characterization of sonochemically prepared proteinaceous microspheres. Ultrason Sonochem. 1994;1(1):S65-8. https://doi.org/10.1016/1350-4177(94)90030-2 DOI: https://doi.org/10.1016/1350-4177(94)90030-2

Silva R, Ferreira H, Azoia NG, Shimanovich U, Freddi G, Gedanken A, et al. Insights on the mechanism of formation of protein microspheres in a biphasic system Mol Pharm. 2012;9(11):3079-88. https://doi.org/10.1021/mp3001827 PMid:23025530 DOI: https://doi.org/10.1021/mp3001827

Ter Haar GR, Robertson D. Tissue destruction with focused ultrasound in vivo. Eur Urol 1993;23(suppl 1):8-11. https://doi.org/10.1159/000474672 PMid:8513833 DOI: https://doi.org/10.1159/000474672

Meng Y, Pople CB, Budiansky D, Li D, Suppiah S, Lim-Fat MJ, et al. Current state of therapeutic focused ultrasound applications in neuro-oncology. J Neurooncol. 2022;156(1):49-59. https://doi.org/10.1007/s11060-021-03861-0 PMid:34661791 DOI: https://doi.org/10.1007/s11060-021-03861-0

Beisteiner R, Matt E, Fan C, Baldysiak H, Schönfeld M, Novak TP. Transcranial pulse stimulation with ultrasound in Alzheimer’s disease-a new navigated focal brain therapy. Adv Sci (Weinh). 2020;7(3):1902583. https://doi.org/10.1002/advs.201902583 PMid:32042569 DOI: https://doi.org/10.1002/advs.201902583

Matt E, Kaindl L, Tenk S, Egger A, Kolarova T, Karahasanović N, et al. First evidence of long-term effects of transcranial pulse stimulation (TPS) on the human brain. J Transl Med. 2022;20(1):26. https://doi.org/10.1186/s12967-021-03222-5 PMid:35033118 DOI: https://doi.org/10.1186/s12967-021-03222-5

Matt E, Dörl G, Beisteiner R. Transcranial pulse stimulation (TPS) improves depression in AD patients on state-of-the-art treatment. Alzheimer’s Dement (N Y). 2022;8(1):e12245. https://doi.org/10.1002/trc2.12245 PMid:35169611 DOI: https://doi.org/10.1002/trc2.12245

Cont C, Stute N, Galli A, Schulte C, Logmin K, Trenado C, et al. Retrospective real-world pilot data on transcranial pulse stimulation in mild to severe Alzheimer’s patients. Front Neurol. 2022;13:948204. https://doi.org/10.3389/fneur.2022.948204 PMid:36188380 DOI: https://doi.org/10.3389/fneur.2022.948204

Radjenovic S, Dörl G, Gaal M, Beisteiner R. Safety of clinical ultrasound neuromodulation. Brain Sci. 2022;12(10):1277. https://doi.org/10.3390/brainsci12101277 PMid:36291211 DOI: https://doi.org/10.3390/brainsci12101277