JBBS> Vol.2 No.1, February 2012

Endovascular Application of Low-Energy Laser in the Treatment of Dyscirculatory Angiopathy of Alzheimer’s Type

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ABSTRACT

Purpose: We propose an analysis of dyscirculatory angiopathy of Alzheimer’s type (DAAT) endovascular treatment method based on transcatheter revascularization and recovery of collateral and microvascular bed of the brain by means of low-energy transluminal laser irradiation as well as its comparison with traditional Alzheimer’s disease (AD) treatment methods. Methods: The research involved 81 patients aged 34 - 79 (average age 67). 46 (46.8%) patients were treated using endovascular method—Test Group. 35 (43.2%) patients were given conventional treatment—Control Group. Patients were subdivided: Group (CDR-0): 9 (11.1%), pre-clinical stage or increased AD risk; Group (CDR-1): 24 (29.6%), mild dementia and cognitive impairment; Group (CDR-2): 31 (38.3%), moderate dementia and persistent cognitive impairment; Group (CDR-3): 17 (21.0%), severe dementia and cognitive impairment. Research plan included CT or MRI with subsequent temporal lobes volume calculation, brain scintigraphy (SG), rheoencephalography (REG), and cerebral MUGA. There were indications and contraindications for treatment in Test Group. In Group CDR-0, endovascular intervention was prophylactic, against the background of increasing memory impairment; in Groups CDR-1, CDR-2, CDR-3, it was conducted in 1 to 12 years period from AD symptoms appear-ance. Conservative treatment with Memantin and Rivastigmine was carried out in Control Group. Results: In Test Group, positive outcome accompanied by prolonged dementia decline, cognitive impairment decrease, and patients’ transition to CDR group of an earlier stage, was obtained in all cases. In Control Group, patients’ temporary stabilization in their own CDR group was achieved. Conclusions: Endovascular treatment of patients with AD different stages can not only reduce DAAT phenomena but can also cause AD regression possibly accompanied by regenerative processes in the cerebral tissue. Conservative treatment only allows stabilizing the patient’s condition for a while.

Cite this paper

I. Maksimovich, "Endovascular Application of Low-Energy Laser in the Treatment of Dyscirculatory Angiopathy of Alzheimer’s Type," Journal of Behavioral and Brain Science, Vol. 2 No. 1, 2012, pp. 67-81. doi: 10.4236/jbbs.2012.21008.

References

[1] Alzheimer’s Disease Facts and Figures, 2007. A Statistical Abstract of US Data on Alzheimer’s Disease published by the Alzheimer’s Association. http://www.alz.org/national/documents/Report_2007FactsAndFigures.pdf
[2] Alzheimer’s Disease Facts and Figures, Alzheimer’s Association, 2010. http://www.alz.org/documents_custom/report_alzfactsfigures2010.pdf
[3] Generation Alzheimer’s: The Defining Disease of the Baby Boomers. http://act.alz.org/site/DocServer/ALZBoomersReport.pdf?docID=521
[4] Alzheimer’s Disease Facts and Figures, 2011. http://www.alz.org/downloads/Facts_Figures_2011.pdf
[5] R. Altman and J. C. Rutledge, “The Vascular Contribution to Alzheimer’s Disease,” Clinical Science, Vol. 119, 2010, pp. 407-421. doi:10.1042/CS20100094 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950620/?tool=pubmed
[6] R. A. Sperling, P. S. Aisen, L. A. Beckett, et al., “Toward Defining the Preclinical Stages of Alzheimer’s Disease: Recommendations from the National Institute on Aging-Alzheimer’s Association Workgroups on Diagnostic Guidelines for Alzheimer’s Disease,” Journal of Alzheimer’s & Dementia, Vol. 7, No. 3, 2011, pp. 280-292. http://www.alzheimersanddementia.com/article/S1552-5260(11)00099-9/abstract
[7] A. Fagan, C. Xiong, R. Bateman, et al., “Plasma and Cerebrospinal Fluid Markers in the DIAN Study of Autosomal-Dominant Alzheimer’s Disease,” Journal of Alzheimer’s & Dementia, Vol. 7, No. 4, 2011, p. 287. http://www.alzheimersanddementia.com/article/S1552-5260(11)00972-1/fulltext
[8] R. J. Perrin, R. Craig-Schapiro, J. C. Morris, et al., “Identification and Validation of Novelcerebrospinal Fluid Biomarkers for Staging Early Alzheimer’s Disease,” Public Library of Science One, Vol. 12, No. 6, 2011, p. e16032. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3020224/?tool=pmcentrez
[9] B. C. Dickerson, “Functional Magnetic Resonance Imaging of Cholinergic Modulation in Mild Cognitive Impairment,” Current Opinion in Psychiatry, Vol. 19, 2006, pp. 299-306. doi:10.1097/01.yco.0000218602.25346.c6 http://www.nmr.mgh.harvard.edu/~bradd/dickerson_curropnpsych_2006.pdf
[10] A. J. Saykin, H. A. Wishart, L. A. Rabin, et al., “Older Adults with Cognitive Complaints Show Brain Atrophy Similar to That of Amnestic MCI,” Neurology, Vol. 67, 2006, pp. 834-842. doi:10.1212/01.wnl.0000234032.77541.a2 http://www.neurology.org/cgi/content/abstract/67/5/834
[11] W. S. Tae, S. S Kim, K. U. Lee, et al., “Validation of Hippocampal Volumes Measured Usinga a Manual Method and Two Automated Methods (Free Surfer and IBASPM) in Chronic Major Depressive Disorder,” Neuroradiology, Vol. 50, 2008, pp. 569-581. doi:10.1007/s00234-008-0383-9 http://www.ncbi.nlm.nih.gov/pubmed/18414838
[12] I. V. Maksimovich, L. N. Gotman and S. M. Masyuk, “Method of Determining Dimensions of Temporal Brain Lobes in Patients Suffering from Alzheimer’s Disease,” Russian Patent, No 2306102, 2006. http://worldwide.espacenet.com/publicationDetails/biblio?DB=EPODOC&adjacent=true&locale=en_EP&FT=D&date=20070920&CC=RU&NR=2306102C1&KC=C1
[13] S. L. Risacher, A. J. Saykin, J. D. West, et al., “Baseline MRI Predictors of Conversion from MCI to Probable AD in the ADNI Cohort,” Current Alzheimer Research, Vol. 6, No. 4, 2009, pp. 347-361. doi:10.2174/156720509788929273 http://www.bentham.org/car/openaccssearticles/car6-4/0007.pdf
[14] L. Shen, H. A. Firpi, A. J. Saykin, et al., “Parametric Surface Modeling and Registration for Comparison of Manual and Automated Segmentation of the Hippocampus,” Hippocampus, Vol. 19, No. 6, 2009, pp. 588-595. doi:10.1002/hipo.20613 http://picsl.upenn.edu/caph08/papers/paper07.pdf
[15] G. Waldemar, B. Dubois, M. Emre, et al., “Recommendations for the Diagnosis and Management of Alzheimer’s Disease and Other Disorders Associated with Dementia: EFNS Guideline,” European Journal of Neurology, Vol. 14, No. 1, 2007, pp. e1-e26. doi:10.1111/j.1468-1331.2006.01605.x http://www.ncbi.nlm.nih.gov/pubmed/17222085
[16] I. V. Maksimovich, “Possibilities of Modern Computed Tomography of Brain in Alzheimer’s Disease Diagnosis,” The Neurologic Bulletin, Vol. XLI, No. 1, 2009, pp. 5-10. http://www.infamed.com/nb/1_2009_5-10.pdf
[17] S. Adriaase, E. Sanz-Arigita, M. Binnewijzend, et al., “Molecular Markers of Alzheimer’s Disease Pathology and Their Relationship with Default Mode Network Integrity,” Alzheimer’s & Dementia, Vol. 7, No. 4, 2011, pp. S2-S3. doi:10.1016/j.jalz.2011.05.005 http://www.alzheimersanddementia.com/article/S1552-5260(11)00144-0/fulltext
[18] C. Jack, P. Vemuri, H. Viste, et al., “Ordering of Alzheimer’s Disease Biomarkers,” Alzheimer’s & Dementia, Vol. 7, No. 4, 2011, pp. S4-S5. doi:10.1016/j.jalz.2011.05.011 http://www.alzheimersanddementia.com/article/S1552-5260(11)00150-6/images
[19] J. Q. Trojanowski, H. Vandeerstichele, M. Korecka, et al., “Update on the Biomarker Core of the Alzheimer’s Disease Neuroimaging Initiative Subjects,” Alzheimer’s & Dementia, Vol. 6, No. 3, 2010, pp. 230-238. doi:10.1016/j.jalz.2010.03.008 http://www.ncbi.nlm.nih.gov/pubmed/20451871
[20] P.T. Meyer, S. Hellwig, F. Amtage, et al., “Dual-Biomarker Imaging of Regional Cerebral Amyloid Load and Neuronal Activity in Dementia with PET and 11C-Labeled Pittsburgh Compound B,” Journal of Nuclear Medicine, Vol. 52, No. 3, 2011, pp. 393-400. doi:10.2967/jnumed.110.083683 http://www.ncbi.nlm.nih.gov/pubmed/21321269
[21] F. Morel “An Apparently Dyshoric and Topical Angiopathy,” Monatsschrift für Psychiatrie und Neurologie, Vol. 120, No. 5-6, 1950, pp. 352-357. doi:10.1159/000140150 http://www.ncbi.nlm.nih.gov/pubmed/14806299
[22] I. Skoog, R. N. Kalaria and M. M. Breteler, “Vascular Factors and Alzheimer Disease,” Alzheimer Disease and Associated Disorders, Vol. 13, No. 3, 1999, pp. 106-114. doi:10.1097/00002093-199912003-00016 http://www.ncbi.nlm.nih.gov/pubmed?term=Skoog%20I%2C%20Kalaria%20R%20N%2C%20Breteler%20M.M.
[23] R. N. Kalaria, “Small Vessel Disease and Alzheimer’s Dementia: Pathological Considerations,” Cerebrovascular Diseases, Vol. 13 No. 2, 2002, pp. 48-52. doi:10.1159/000049150 http://www.ncbi.nlm.nih.gov/pubmed/11901243
[24] R. N. Kalaria, “Vascular Factors in Alzheimer’s Disease,” International Psychogeriatric, Vol. 15, No. 1, 2003, pp. 47-52. doi:10.1017/S1041610203008950 http://www.ncbi.nlm.nih.gov/pubmed/16191216
[25] I. V. Maksimovich, “Changes in Angioarchetectonics of Brain at Alzheimer’s Disease,” The Neurological Bulletin, Vol. XLI, No. 2, 2009, pp. 9-14. http://www.infamed.com/nb/2_2009_9-14.pdf
[26] P. A. Yates, R. Sirisriro, V. L. Villemagne, et al., “Cerebral Microhemorrhage and Brain {beta}-amyloid in Aging and Alzheimer’s Disease,” Neurology, Vol. 77, No. 1, 2011, pp. 48-54. doi:10.1212/WNL.0b013e318221ad36 http://www.ncbi.nlm.nih.gov/pubmed/21700585
[27] I. V. Maksimovich, “Radiodiagnostics of Alzheimer’s disease,” Diagnostics and Intervention Radiology, Vol. 2, No. 4, 2008, pp. 27-38. http://www.radiology-di.ru/articles/155/126/tom-2-N4-2008.html
[28] G. Rodriguez, P. Vitali, P. Calvini, C. Bordoni, N. Girtler, G. Taddei, G. Mariani and F. Nobili, “Hippocampal Perfusion in Mild Alzheimer’s Disease,” Psychiatry Research, Vol. 100, No. 2, 2000, pp. 65-74. doi:10.1016/S0925-4927(00)00071-8 http://www.ncbi.nlm.nih.gov/pubmed/11114492
[29] W. Chen, X. Song, S. Beyea, R. D’Arcy, Y. Zhan and K. Rockwood, “Advances in Perfusion Magnetic Resonance Imaging in Alzheimer’s Disease,” Journal of Alzheimer’s & Dementia, Vol. 7, No. 2, 2011, pp. 185-196. http://www.alzheimersanddementia.com/article/S1552-5260(10)00105-6/abstract
[30] R. O. Weller, M. Subash, S. D. Preston, I. Mazanti and R. O. Carare, “Perivascular Drainage of Amyloid-beta Peptides from the Brain and Its Failure in Cerebral Amyloid Angiopathy and Alzheimer’s Disease,” Brain Pathology, Vol. 18, No. 2, 2008, pp. 253-266. doi:10.1111/j.1750-3639.2008.00133.x http://www.ncbi.nlm.nih.gov/pubmed/18363936
[31] A. Pezzini, E. Del Zotto, I. Volonghi, A. Giossi, P. Costa and A. Padovani, “Cerebral Amyloid Angiopathy: A Common Cause of Cerebral Hemorrhage,” Current Medicinal Chemistry, Vol. 16, No. 20, 2009, pp. 2498-2513. doi:10.2174/092986709788682047 http://www.ncbi.nlm.nih.gov/pubmed/19601795
[32] Y. A. Chung, O. J. Hyun, J. Y. Kim, K. J. Kim and K. J. Ahn, “Hypoperfusion and Ischemia in Cerebral Amyloid Angiopathy Documented by 99mTc-ECD Brain Perfusion SPECT,” Journal of Nuclear Medicine, Vol. 50, No. 12, 2009, pp. 1969-1974. doi:10.2967/jnumed.109.062315 http://www.ncbi.nlm.nih.gov/pubmed/19910418
[33] R. O. Weller, S. D. Preston, M. Subash and R. O. Carare, “Cerebral Amyloid Angiopathy in the Aetiology and Immunotherapy of Alzheimer’s Disease,” Alzheimer’s Research & Therapy, Vol. 1, No. 2, 2009, pp. 6-13. http://www.ncbi.nlm.nih.gov/pubmed/19822028
[34] I. V. Maksimovich and L. N. Gotman, “Method of Complex Radiation Diagnostics at Pre-clinical and Clinical Stages of Alzheimer’s Disease,” Russian Patent, No. 2315559, 2006. http://bankpatentov.ru/node/28577
[35] I. V. Maksimovich, “Dyscirculatory Angiopathy of the Brain of Alzheimer’s Type,” Journal of Alzheimer’s & Dementia, Vol. 6, No. 4, 2010, pp. e34-e35. http://www.alzheimersanddementia.com/article/S1552-5260(10)02300-9/fulltext
[36] I. V. Maksimovich, “Dyscirculatory Angiopathy of Alzheimer’s Type,” Journal of Behavioral and Brain Science, Vol. 1, No. 2, 2011, pp. 57-68. doi:10.4236/jbbs.2011.12008 http://www.scirp.org/journal/PaperInformation.aspx?paperID=4630
[37] D. Wilkinson, “Drugs for Treatment of Alzheimers’ Disease,” International Journal of Clinical Practice, Vol. 55. No. 2, 2001, pp. 129-134. http://www.ncbi.nlm.nih.gov/pubmed/11321852
[38] S. Burgmans, M. P. Van Boxtel, E. F. Vuurman, F. Smeets, E. H. Gronenschild, H. B. Uylings and J. Jolles, “The Prevalence of Cortical Gray Matter Atrophy May Be Overestimated In the Healthy Aging Brain,” Neuropsychology, Vol. 23, No. 5, 2009, pp. 541-550. doi:10.1037/a0016161 http://www.ncbi.nlm.nih.gov/pubmed/19702408
[39] G. C. Chiang, Ph. S. Insel, D. Tosun, N. Schuff, D. Truran-Sacrey, S. Raptentsetsang, C. R. Jack and M. W. Weiner, “Identifying Cognitively Healthy Elderly Individuals with Subsequent Memory Decline by using Automated MR Temporoparietal Volumes,” Radiology, Vol. 259, No. 3, 2011, pp. 844-851. doi:10.1148/radiol.11101637 http://www.ncbi.nlm.nih.gov/pubmed/21467255
[40] J. C. Morris, “The Clinical Dementia Rating (CDR): Current Version and Scoring Rules,” Neurology, Vol. 11, No. 43, 1993, pp. 2412-2414. http://www.neurology.org/content/43/11/2412.2.full.pdf+html
[41] I. V. Maksimovich, “Method for Endovascular Treatment of Alzheimer’s Disease,” Russian Patent, No. 2297860, 2006. http://worldwide.espacenet.com/publicationDetails/originalDocument?FT=D&date=20070427&DB=EPODOC& locale=en_EP&CC=RU&NR=2297860C1&KC=C1
[42] I. V. Maksimovich, “Method and Device for Endovascular Treatment of Alzheimer’s Disease,” Patent US, No. 7389776, 2008. http://www.freepatentsonline.com/7389776.pdf
[43] I. V. Maksimovich, “Endovascular Procedures in Treatment of the Alzheimer’s Disease,” Journal Diagnostic and Intervention Radiology, Vol. 3, No. 2, 2009, pp. 23-35. http://www.radiology-di.ru/articles/158/177/tom-3-N2-2009.html
[44] I. V. Maksimovich, “Endovascular Low-Energy Laser Radiation Effect on Dyscirculatory Angiopathy of Alzheimer’s Type in the Treatment of Alzheimer’s Disease,” Journal of Alzheimer’s & Dementia, Vol. 7, No. 4, 2011, pp. S791-S793. http://www.alzheimersanddementia.com/article/S1552-5260(11)02427-7/fulltext
[45] A. Venneri, M. F. Shanks, R. T. Staff, et al., “Cerebral Blood Flow and Cognitive Responses to Rivastigmine Treatment in Alzheimer’s Disease,” Neuroreport, Vol. 13, No. 1, 2002, pp. 83-87. . doi:10.1097/00001756-200201210-00020 http://www.ncbi.nlm.nih.gov/pubmed/11924899
[46] A. Fredriksson, W. Danysz, G. Quack, et al., “Coadministration of Memantine and Amantadine with Sub/supratheshold Doses of L-Dopa Restores Motor Behaviour of MPTP-Treated Mice,” Journal of Neural Transmission, Vol. 108, No. 2, 2001, pp. 167-187. doi:10.1007/s007020170086 http://www.ncbi.nlm.nih.gov/pubmed?term=Fredriksson%20A%2C%20Danysz%20W%2C%20Quack%20G%2C%20et%20al
[47] D. Wilkinson, “Drugs for Treatment of Alzheimer’s Disease,” International Journal of Clinical Practice, Vol. 55, No. 2, 2001, pp. 129-134. http://www.ncbi.nlm.nih.gov/pubmed/11321852
[48] I. V. Maksimovich, “Transljuminal Laser Angioplasty in Treatment of Ischemic Lesions of a Brain,” M.D. Dissertation, Russian University of Friendship of the People, Moscow, 2004. http://disseng.com/page/order/id/206426.html
[49] G. K. Chizhov, N. I. Koval’skaia and V. I. Kozlov, “The Effect of Helium-Neon Laser Radiation on the Energy Metabolic Indices of the Myocardium,” Biulleten’ Eksperimental’no? Biologii i Meditsiny, Vol. 111, No. 3, 1991, pp. 302-305. http://www.ncbi.nlm.nih.gov/pubmed/2054512
[50] V. I. Kozlov and G. A. Aziziv, “Pathophysiological Characteristics of Microcirculatory Disorders in Chronic Arterial Ischaemia of Lower Limbs,” Angiology and Vascular Surgery, Vol. 13, No. 7, 2007, pp. 17-23. http://www.ncbi.nlm.nih.gov/pubmed/17679971
[51] S. V. Moskvin, “System Analysis of Efficiency in Controlling Biological Systems with Low-Energy Laser Radiation,” Thesis for Degree of Doctor of Biological Sciences, City of Tula, 2008. http://www.dissers.info/disser_323120.html
[52] Ch. Heinrich, R. Blum, S. Gascón, et al., “Directing Astroglia from the Cerebral Cortex into Subtype Specific Functional Neurons,” PLoS Biology, Vol. 8, No. 5, 2010, p. e1000373. doi:10.1371/journal.pbio.1000373 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872647/?tool=pmcentrez

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