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

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.

Dyscirculatory Angiopathy of Alzheimer's Type

Purpose: We assess the significance of dyscirculatory angiopathy of Alzheimer’s type (DAAT) in identify- ing the predisposition to the development and diagnosis of Alzheimer’s disease (AD) different stages. Meth- ods: 108 patients took part in the research:1) 49 aged 34-79 suffering from AD or running an increased risk of its development (those not diagnosed with AD but having growing memory disorders without any mani- festations of dementia or specific cognitive impairments, and having 2 or more immediate relatives with AD) - Test Group;2) 59 aged 28-78 suffering from different types of brain lesions accompanied by dementia but not suffering from AD or corresponding to their age norm - Control Group. All the patients underwent MRI, CT with subsequent calculation of the temporal lobes atrophy degree, brain scintigraphy (SG), rheoencepha- lography (REG), and MUGA. Results: Characteristic features of patients with an increased risk of AD as well as at its various stages are: 1) Temporal lobes and hippocampus atrophy ranging from 4% among those with an increased risk of AD to 62% among those at its advanced stages;2) DAAT manifestations: reduction of the capillary bed in the temporal and frontoparietal regions with the development of multiple arterioven- ous shunts of the same localization and correspondent early venous discharge accompanied by venous stasis on the border of the frontal and parietal region;3) DAAT phenomena equally develop both among those with an increased risk of developing AD and those at various AD stages. Similar changes are not observed among Control Group patients with other brain lesions, regardless of the severity of dementia, as well as among practically healthy people of the corresponding age group. Conclusion: Timely identification of the above- mentioned changes can reveal a predisposition to AD development long before its initial manifestations, and it allows differentiating AD from other diseases attended by dementia. In both cases, timely diagnosis allows beginning timely treatment and thus achieving more stable results.

Dementia and Cognitive Impairment Reduction after Laser Transcatheter Treatment of Alzheimer’s Disease

Reduced cerebral perfusion and microcirculation are found among AD causes, which should be considered in the development of new treatments for the disease. 165 patients with AD were examined. The examination plan included clinical assessment of dementia severity (CDR), cognitive function assessment (MMSE), laboratory examination, cerebral scintigraphy (SG), rheoencephalography (REG), cerebral CT and MRI, morphometric AD stages assessment (TDR) and cerebral multi-gated angiography (MUGA). 89 patients aged 34 - 79 (average age 67) were selected for the treatment: 31 (34.83%) male, 58 (65.17%) female patients. According to their AD stage, the patients were divided into: TDR-0 (preclinical stage)—10 (11.24%) patients, TDR-1 (early stage with mild dementia, mild cognitive impairment)—28 (31.46%) patients, TDR-2 (medium stage with moderate dementia, cognitive impairment sufficiently persistent)—34 (38.20%) patients, TDR-3 (late stage with sufficiently severe dementia and cognitive impairment)—17 (19.10%) patients. Test Group—46 (51.68%) patients—had transcatheter treatment with low-energy lasers. Control Group—43 (48.31%)—had conservative treatment with Memantin and Rivastigmine. The Test Group had cerebral microcirculation improvement leading to permanent dementia reduction and cognitive recovery which allowed transferring the patients to a lighter TDR group or withdrawing them from the scale. Control Group patients with earlier AD stages (TDR-0, TDR-1, TDR-2) obtained stabilization for a period of 6 months-3 years, with subsequent growth of dementia and cognitive impairment;patients with late AD stage (TDR-3) showed further increase of cognitive impairment and dementia. Transcatheter treatment allows reducing the effects of dyscirculatory angiopathy of Alzheimer’s type (DAAT) improving cerebral microcirculation and metabolism, which leads to permanent dementia regression and cognitive impairment reduction. These data show that AD treatment should be comprehensive and aimed at both the recovery of cerebral microcirculation and blood supply and the normalization of amyloid beta metabolism in the cerebral tissue.

Disorders of cerebrovascular angioarchitectonics and microcirculation in the etiology and pathogenesis of Alzheimer’s disease

There have recently appeared many reports dedicated to cerebral hemodynamics disorders in AD. However, certain specific aspects of cerebral blood flow and microcirculation during this disease are not fully understood. This research focuses on the identification of particular features of cerebral angioarchitectonics and microcirculation at preclinical and clinical AD stages and on the determination of their importance in AD etiology and pathogenesis. 164 patients participated in the research: Test Group—81 patients with different AD stages;Control Group— 83 patients with etiologically different neurodegenerative brain lesions with manifestations of dementia and cognitive impairment but without AD. All patients underwent: assessment of cognitive function (MMSE), severity of dementia (CDR) and AD stages (TDR), laboratory examination, computed tomography (CT), magnetic resonance imaging (MRI), brain scintigraphy (SG), rheoencephalography (REG) and cerebral multigated angiography (MUGA). All Test Group patients, irrespective of their AD stage, had abnormalities of the cerebral microcirculation manifested in dyscirculatory angiopathy of Alzheimer’s type (DAAT), namely: reduction of the capillary bed in the hippocampus and frontal-parietal regions;development of multiple arteriovenous shunts in the same regions;early venous dumping of arterial blood through these shunts with simultaneous filling of arteries and veins;development of abnormally enlarged lateral venous trunks that receive blood from the arterio-venous shunts;anomalous venous congestion at the border of frontal and parietal region;increased loop formation of distal intracranial arterial branches. Control group patients did not have combinations of such changes. These abnormalities are specific for AD and can affect amyloid beta metabolism contributing to its accumulation in the brain tissue and thereby stimulating AD progression.

Certain new aspects of etiology and pathogenesis of Alzheimer’s disease

The research focuses on the possibility of early detection of AD-specific vascular and atrophic brain changes in families which have a tendency to inherit the disease. The research includedthree families with AD inheritance. All patientsunderwent: cognitive function assessment(MMSE),determination of dementia severity(CDR) and AD stages (TDR), computed tomography (CT), magnetic resonance imaging (MRI), scintigraphy of the brain (SG), rheoencephalography (REG), and cerebral multigated angiography (MUGA). All patients with different AD stages, as well as their descendants, have specific atrophic changes in the temporal lobes of the brain. The degree of these changes increases as AD becomes more severe and ranges from 4% - 8% (TDR-0) to 33% - 62% (TDR-3) of the total mass of a healthy person’s temporal lobes. Simultaneously, thepatients examined have changes of microcirculation manifested by reduction of the capillarybed in the temporal and frontalparietal regions,the development of multiple arteriovenousshunts in the same areas, early venous dumping, anomalous expansion of venoustrunks that receive blood from the arterialvenous shunts, venous stasis on the frontoparietal boundary. Similar changes are found among AD patients’ descendants aged 8 - 11, the only difference being in the degree of temporal lobes atrophy which is 4.7%. This proves that microcirculatory disorders are primary and atrophic changes of the temporal lobes are secondary in AD development. The data obtained indicate that the examination of AD patients’ relatives should begin well before the possible manifestations of the disease, even in childhood. It will allow to reveal the possibility of inheritance and the signs of the disease at the earliest possible stage and to begin its treatment in time.

Vascular factors in Alzheimer’s disease

The vascular factor in Alzheimer’s disease (AD), affecting its development and progression, is one of the most urgent problems of modern neuroangiology. The research investigates the characteristics of cerebral angioarchitectonics identified at different stages of AD. The research included 106 patients: 1) The Test Group—47 patients suffering from various stages of AD;2) The Control Group—59 patients suffering from the most common lesions of the brain accompanied by neurodegenerative changes, the development of dementia and cognitive impairment, but not having AD. All the patients underwent: the testing of cognitive functions (MMSE), the determination of severity of dementia (CDR) and AD stages (TDR), computed tomography (CT), magnetic resonance imaging (MRI), scintigraphy of the brain (SG), rheoencephalography (REG), and cerebral multigated angiography (MUGA). Patients with AD different stages showed the following changes in angioarchitectonics and microcirculation: Absence of pronounced atherosclerotic lesions of intracranial vessels, reduction of the capillary bed in the temporal and temporo-parietal regions, development of multiple arteriovenous shunts in the same areas, early venous discharge, abnormal expansion of venous trunks that receive blood from arteriovenous shunts, venous congestion at the border of the frontal and parietal region, increased looping of intracranial arteries. Control Group patients had no combination of the abovementioned changes. These vascular changes are specific for AD and are in fact the vascular factor of this disease;they may also be called dyscirculatory angiopathy of Alzheimer’s type (DAAT). Patients suffering from other diseases that are accompanied by neurodegenerative changes in the brain, dementia and cognitive impairment do not have them.

Differences in Cerebral Angioarchitectonics in Alzheimer’s Disease in Comparison with Other Neurodegenerative and Ischemic Lesions

Introduction: The research focuses on the clinical study of cerebral angioarchitectonics and microcirculation disorders in the development of Alzheimer’s disease (AD) in comparison with other neurodegenerative and ischemic lesions. Materials and methods: 1117 patients with different types and stages of neurodegenerative and ischemic lesions were examined, 93 of whom (8.33%) had different stages of AD—Test Group;1024 (91.67%) had cerebral atherosclerosis, Binswanger disease (BD), vascular Parkinsonism (VP)—Control Group. The examination included definition of CDR, MMSE, cerebral CT, MRI, cerebral sciagraphy (SG), rheoencephalography (REG), morphometric detection of AD stages with TDR, and cerebral multi-gated angiography (MUGA). Results: In all patients with AD, regardless of the disease stage, specific сerebral small vessel disease (CSVD), manifested by dyscirculatory angiopathy of Alzheimer’s type (DAAT), was detected in the temporal and fronto-parietal areas. Conclusions: DAAT is an AD-specific lesion of cerebral microvessels that changes hemodynamics, causes cerebral hypoxia, and contributes to impaired amyloid beta metabolism. The combination of deposition of amyloid beta in the cerebral tissue and vascular wall, as well as specific disorders of microcirculation, cause neurodegeneration and AD development. Patients with other neurodegenerative and ischemic lesions had no DAAT manifestations.