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Provenzano, F.A., Muraskin, J., Tosto, G., Narkhede, A., Wasserman, B.T., Griffith, E.Y., Guzman, V.A., Meier, I.B., Zimmerman, M.E. and Brick-man, A.M. (2013) White matter hyperintensities and cerebral amyloidosis: Necessary and sufficient for clinical expression of Alzheimer disease? JAMA Neurology, 70, 455-461. http://www.ncbi.nlm.nih.gov/pubmed/23420027

has been cited by the following article:

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

  AUTHORS: Ivan V. Maksimovich

  KEYWORDS: Alzheimer’s Disease; Dementia, TDR; Microcirculation; Microcirculatory Disorders; Dyscirculatory Angiopathy of Alzheimer’s Type; DAAT

  JOURNAL NAME: Advances in Alzheimer's Disease, Vol.2 No.4, December 4, 2013

  ABSTRACT: 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.