Hunter, J.M., Kwan, J., Malek-Ahmadi, M., Maarouf, C.L., Kokjohn, T.A., Belden, C., Sabbagh, M.N., Beach, T.G. and Roher, A.E. (2012) Morphological and pathological evolution of the brain microcirculation in aging and Alzheimer’s disease. PLoS One, 7, e36893. http://www.ncbi.nlm.nih.gov/pubmed?term=%5B30%5D%09Hunter%2C%20J.%20M.%20Kwan%2C%20J%20%20Malek-Ahmadi%2C%20M.%20Maarouf%2C%20C.%20L.%20Kokjohn%2C%20T.%20A.%20Belden%2C%20C.%20Sabbagh%2C%20M.%20N.%20Beach%2C%20T.G.%20Roher%2C%20A.%20E.%20(2012)%20Mor

has been cited by the following article:

• TITLE: Vascular factors in Alzheimer’s disease

  AUTHORS: Ivan V. Maksimovich

  KEYWORDS: Alzheimer’s Disease; CDR; TDR; Dementia; Vascular Factors in Alzheimer’s Disease; Dyscirculatory Angiopathy of Alzheimer’s Type; DAAT

  JOURNAL NAME: Health, Vol.4 No.9A, September 28, 2012

  ABSTRACT: 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.