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4 results

  • Brain Arterial Diameters and Cognitive Performance: The Northern Manhattan Study

  • Jose Gutierrez, Erin Kulick, Yeseon Park Moon, Chuanhui Dong, Ken Cheung, Bagci Ahmet, Yaakov Stern, Noam Alperin, Tatjana Rundek, Ralph L. Sacco, Clinton B. Wright, Mitchell S.V. Elkind
  • Journal:
    Journal of the International Neuropsychological Society / Volume 24 / Issue 4 / April 2018
    Published online by Cambridge University Press:
    23 November 2017, pp. 335-346

  • Objectives: To test the hypothesis that brain arterial diameters are associated with cognitive performance, particularly in arteries supplying domain-specific territories. Methods: Stroke-free participants in the Northern Manhattan Study were invited to have a brain MRI from 2003–2008. The luminal diameters of 13 intracranial arterial segments were obtained using time-of-flight magnetic resonance angiogram (MRA), and then averaged and normalized into a global score and region-specific arterial diameters. Z-Scores for executive function, semantic memory, episodic memory and processing speed were obtained at MRI and during follow-up. Adjusted generalized additive models were used to assess for associations. Results: Among the 1034 participants with neurocognitive testing and brain MRI, there were non-linear relationships between left anterior (ACA) and middle cerebral artery (MCA) diameter and semantic memory Z-scores (χ2=10.00; DF=3; p=.019), and left posterior cerebral artery (PCA) and posterior communicating artery (Pcomm) mean diameter and episodic memory Z-scores (χ2=9.88; DF=3; p=.020). Among the 745 participants who returned for 2nd neuropsychological testing, on average 5.0±0.4 years after their MRI, semantic memory change was associated non-linearly with the left PCA/Pcomm mean diameter (χ2=13.09; DF=3; p=.004) and with the right MCA/ACA mean diameter (χ2=8.43; DF=3; p=.03). In both cross-sectional and longitudinal analyses, participants with the larger brain arterial diameters had more consistently lower Z-scores and greater decline than the rest of the participants. Conclusions: Brain arterial diameters may have downstream effects in brain function presenting as poorer cognition. Identifying the mechanisms and the directionality of such interactions may increase the understanding of the vascular contribution to cognitive impairment and dementia. (JINS, 2018, 24, 335–346)

  • Chapter 19 - Cerebral microbleeds and antithrombotictreatment

  • from Section 3 - Microbleeds in relation to specific populations, diseases and neurological symptoms
  • Edited by David J. Werring, Institute of Neurology, London
  • Book:
    Cerebral Microbleeds
    Published online:
    05 July 2011
    Print publication:
    26 May 2011, pp 165-172

  • Summary

    This chapter reviews the pathophsyiology and pathology of hypertensive arteriopathy of the brain and its relationship to neuroimaging findings, particularly cerebral microbleeds (CMBs). The prevalence of hypertension is highly age dependent. Hypertension-related cerebral diseases include hypertensive encephalopathy, stroke and vascular cognitive impairment. Although the term arteriopathy includes both arteries and arterioles, the chapter focuses on the intrinsic vascular pathology of arterioles in hypertension. Intracranial atherosclerosis of large arteries is more common in hypertension. The presence of hypertensive arteriolosclerosis must be inferred indirectly. Hypertension is a common age-related disease that is accompanied by loss of vascular integrity, with leakage of red blood cells and perivascular hemosiderin deposition. Cerebral microbleeds caused by hypertensive arteriopathy may be seen in the deep hemispheric regions, brainstem, cerebellum and cerebral lobes; however, the pattern of purely lobar CMBs strongly suggests cerebral amyloid angiopathy (CAA) rather than hypertensive arteriopathy.

  • Chapter 14 - Trophoblast–arterial interactions in vitro

  • from Section 5: - Comparative anatomy and research models
  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 140-148

  • Summary

    The process of endometrial decidualization is a key event with direct relevance to very early pregnancy as well as subsequent pregnancy outcome. This chapter reviews the signals and pathways that control the morphological and biochemical differentiation of resident endometrial fibroblasts into secretory decidual cells. It discusses the functions of these cells at the feto-maternal interface. Decidual transformation of endometrial stromal cells can be faithfully recapitulated in culture and these in vitro studies have yielded invaluable insights into the signal pathways and downstream transcription factors that govern this differentiation process. Decidualizing stromal cells play an important role in local immunomodulation in many ways. The emergence in human beings of a cyclic decidual process has several major clinical implications; the most obvious of which is menstruation and its associated disorders. Decidualizing stromal cells and other cellular components in the superficial endometrial layer take part in menstrual shedding.

  • Chapter 13 - Animal models of deep trophoblast invasion

  • from Section 5: - Comparative anatomy and research models
  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 127-139

  • Summary

    This chapter provides a general overview of the two major components of pregnancy-associated spiral artery remodeling, the maternal (decidual) and the fetal (trophoblastic). During placentation the mother comes in close contact with semi-allogeneic fetal trophoblastic cells which play a key role in maternal-fetal physiological exchange. Focusing on spiral artery invasion, there is little direct evidence for the occurrence of intrinsic trophoblastic defects in early pregnancy. Impaired trophoblast invasion in spiral arteries may not only be due to an intrinsic defect in invasive properties, but may also be induced by maternal cells. For a long time trophoblast invasion was thought to be controlled by a restrictive action of the decidua. A stimulatory role of decidua for trophoblast invasion may also apply to the endovascular invasion of the spiral arteries. Decidua-associated vascular remodeling not only occurs in the decidua but also in the junctional zone myometrial compartment.