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Intracranial pulsatility is associated with regional brain volume in elderly individuals
Umeå University, Faculty of Medicine, Department of Radiation Sciences.
Umeå University, Faculty of Medicine, Department of Radiation Sciences. Umeå University, Faculty of Medicine, Department of Medical Biochemistry and Biophysics.
Umeå University, Faculty of Medicine, Department of Radiation Sciences.
Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience, Clinical Neuroscience.ORCID iD: 0000-0001-6451-1940
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2014 (English)In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 35, no 2, 365-372 p.Article in journal (Refereed) Published
Abstract [en]

Excessive intracranial pulsatility is thought to damage the cerebral microcirculation, causing cognitive decline in elderly individuals. We investigated relationships between brain structure and measures related to intracranial pulsatility among healthy elderly. Thirty-seven stroke-free, non-demented individuals (62-82 years of age) were included. We assessed brain structure, invasively measured cerebrospinal fluid (CSF) pulse pressure, and magnetic resonance-quantified arterial and CSF flow pulsatility, as well as arterial pulse pressure. Using both multivariate partial least squares and ordinary regression analyses, we identified a significant pattern of negative relationships between the volume of several brain regions and measures of intracranial pulsatility. The strongest relationships concerned the temporal lobe cortex and hippocampus. These findings were also coherent with observations of positive relationships between intracranial pulsatility and ventricular volume. In conclusion, elderly subjects with high intracranial pulsatility display smaller brain volume and larger ventricles, supporting the notion that excessive cerebral arterial pulsatility harms the brain. This calls for research investigating altered intracranial cardiac-related pulsatile stress as a potential risk factor that may cause or worsen the prognosis in subjects developing cognitive impairment and dementia.

Place, publisher, year, edition, pages
2014. Vol. 35, no 2, 365-372 p.
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Neurology
Identifiers
URN: urn:nbn:se:umu:diva-98388DOI: 10.1016/j.neurobiolaging.2013.08.026ISI: 000328655600011PubMedID: 24080175OAI: oai:DiVA.org:umu-98388DiVA: diva2:782520
Available from: 2015-01-21 Created: 2015-01-21 Last updated: 2017-12-05Bibliographically approved

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Wåhlin, AndersAmbarki, KhalidBirgander, RichardMalm, JanEklund, Anders

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Wåhlin, AndersAmbarki, KhalidBirgander, RichardMalm, JanEklund, Anders
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