Simultaneous measurement of arterial transit time, arterial blood volume, and cerebral blood flow using arterial spin-labeling in patients with Alzheimer disease

Takashi Yoshiura, Hiwatashi Akio, Koji Yamashita, Y. Ohyagi, A. Monji, Yukihisa Takayama, E. Nagao, H. Kamano, T. Noguchi, Hiroshi Honda

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

BACKGROUND AND PURPOSE: Cerebral hemodynamics abnormality in Alzheimer disease (AD) is not fully understood. Our aim was to determine whether regional hypoperfusion due to AD is associated with abnormalities in regional arterial blood volume (rABV) and regional arterial transit time (rATT) as measured by quantitative arterial spin-labeling (ASL) with multiple-delay time sampling. MATERIALS AND METHODS: Nineteen patients with AD (9 men and 10 women; mean age, 74.5 ± 8.6 years) and 22 cognitively healthy control subjects (11 men and 11 women; mean age, 72.8 ± 6.8 years) were studied by using a quantitative ASL method with multiple-delay time sampling. From the ASL data, maps of regional cerebral blood flow (rCBF), rABV, and rATT were generated. A region of hypoperfusion due to AD was determined by statistical parametric mapping (SPM) analysis. Mean rCBF, rABV, and rATT values within the hypoperfused region were compared between the AD and control groups. RESULTS: Despite the significantly lower rCBF (P = .0004) in patients with AD (27.8 ± 7.1 mL/100 g/min) in comparison with control subjects (36.7 ± 6.3 mL/100 g/min), no significant difference in rATT was observed between the control (0.48 ± 0.09 seconds) and AD (0.47 ± 0.10 seconds) groups. Mean rABV was lower in the AD group (0.22 ± 0.10%) than in the control group (0.27 ± 0.12%), though the difference did not reach the level of statistical significance. CONCLUSIONS: Our results revealed that regional hypoperfusion in AD is not associated with rATT prolongation, suggesting that the mechanism of hypoperfusion is distinct from that in cerebrovascular diseases.

Original languageEnglish
Pages (from-to)1388-1393
Number of pages6
JournalAmerican Journal of Neuroradiology
Volume30
Issue number7
DOIs
Publication statusPublished - Aug 1 2009

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Cerebrovascular Circulation
Blood Volume
Alzheimer Disease
Regional Blood Flow
Cerebrovascular Disorders
Control Groups
Healthy Volunteers
Hemodynamics

All Science Journal Classification (ASJC) codes

  • Radiology Nuclear Medicine and imaging
  • Clinical Neurology

Cite this

Simultaneous measurement of arterial transit time, arterial blood volume, and cerebral blood flow using arterial spin-labeling in patients with Alzheimer disease. / Yoshiura, Takashi; Akio, Hiwatashi; Yamashita, Koji; Ohyagi, Y.; Monji, A.; Takayama, Yukihisa; Nagao, E.; Kamano, H.; Noguchi, T.; Honda, Hiroshi.

In: American Journal of Neuroradiology, Vol. 30, No. 7, 01.08.2009, p. 1388-1393.

Research output: Contribution to journalArticle

Yoshiura, Takashi ; Akio, Hiwatashi ; Yamashita, Koji ; Ohyagi, Y. ; Monji, A. ; Takayama, Yukihisa ; Nagao, E. ; Kamano, H. ; Noguchi, T. ; Honda, Hiroshi. / Simultaneous measurement of arterial transit time, arterial blood volume, and cerebral blood flow using arterial spin-labeling in patients with Alzheimer disease. In: American Journal of Neuroradiology. 2009 ; Vol. 30, No. 7. pp. 1388-1393.
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abstract = "BACKGROUND AND PURPOSE: Cerebral hemodynamics abnormality in Alzheimer disease (AD) is not fully understood. Our aim was to determine whether regional hypoperfusion due to AD is associated with abnormalities in regional arterial blood volume (rABV) and regional arterial transit time (rATT) as measured by quantitative arterial spin-labeling (ASL) with multiple-delay time sampling. MATERIALS AND METHODS: Nineteen patients with AD (9 men and 10 women; mean age, 74.5 ± 8.6 years) and 22 cognitively healthy control subjects (11 men and 11 women; mean age, 72.8 ± 6.8 years) were studied by using a quantitative ASL method with multiple-delay time sampling. From the ASL data, maps of regional cerebral blood flow (rCBF), rABV, and rATT were generated. A region of hypoperfusion due to AD was determined by statistical parametric mapping (SPM) analysis. Mean rCBF, rABV, and rATT values within the hypoperfused region were compared between the AD and control groups. RESULTS: Despite the significantly lower rCBF (P = .0004) in patients with AD (27.8 ± 7.1 mL/100 g/min) in comparison with control subjects (36.7 ± 6.3 mL/100 g/min), no significant difference in rATT was observed between the control (0.48 ± 0.09 seconds) and AD (0.47 ± 0.10 seconds) groups. Mean rABV was lower in the AD group (0.22 ± 0.10{\%}) than in the control group (0.27 ± 0.12{\%}), though the difference did not reach the level of statistical significance. CONCLUSIONS: Our results revealed that regional hypoperfusion in AD is not associated with rATT prolongation, suggesting that the mechanism of hypoperfusion is distinct from that in cerebrovascular diseases.",
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T1 - Simultaneous measurement of arterial transit time, arterial blood volume, and cerebral blood flow using arterial spin-labeling in patients with Alzheimer disease

AU - Yoshiura, Takashi

AU - Akio, Hiwatashi

AU - Yamashita, Koji

AU - Ohyagi, Y.

AU - Monji, A.

AU - Takayama, Yukihisa

AU - Nagao, E.

AU - Kamano, H.

AU - Noguchi, T.

AU - Honda, Hiroshi

PY - 2009/8/1

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N2 - BACKGROUND AND PURPOSE: Cerebral hemodynamics abnormality in Alzheimer disease (AD) is not fully understood. Our aim was to determine whether regional hypoperfusion due to AD is associated with abnormalities in regional arterial blood volume (rABV) and regional arterial transit time (rATT) as measured by quantitative arterial spin-labeling (ASL) with multiple-delay time sampling. MATERIALS AND METHODS: Nineteen patients with AD (9 men and 10 women; mean age, 74.5 ± 8.6 years) and 22 cognitively healthy control subjects (11 men and 11 women; mean age, 72.8 ± 6.8 years) were studied by using a quantitative ASL method with multiple-delay time sampling. From the ASL data, maps of regional cerebral blood flow (rCBF), rABV, and rATT were generated. A region of hypoperfusion due to AD was determined by statistical parametric mapping (SPM) analysis. Mean rCBF, rABV, and rATT values within the hypoperfused region were compared between the AD and control groups. RESULTS: Despite the significantly lower rCBF (P = .0004) in patients with AD (27.8 ± 7.1 mL/100 g/min) in comparison with control subjects (36.7 ± 6.3 mL/100 g/min), no significant difference in rATT was observed between the control (0.48 ± 0.09 seconds) and AD (0.47 ± 0.10 seconds) groups. Mean rABV was lower in the AD group (0.22 ± 0.10%) than in the control group (0.27 ± 0.12%), though the difference did not reach the level of statistical significance. CONCLUSIONS: Our results revealed that regional hypoperfusion in AD is not associated with rATT prolongation, suggesting that the mechanism of hypoperfusion is distinct from that in cerebrovascular diseases.

AB - BACKGROUND AND PURPOSE: Cerebral hemodynamics abnormality in Alzheimer disease (AD) is not fully understood. Our aim was to determine whether regional hypoperfusion due to AD is associated with abnormalities in regional arterial blood volume (rABV) and regional arterial transit time (rATT) as measured by quantitative arterial spin-labeling (ASL) with multiple-delay time sampling. MATERIALS AND METHODS: Nineteen patients with AD (9 men and 10 women; mean age, 74.5 ± 8.6 years) and 22 cognitively healthy control subjects (11 men and 11 women; mean age, 72.8 ± 6.8 years) were studied by using a quantitative ASL method with multiple-delay time sampling. From the ASL data, maps of regional cerebral blood flow (rCBF), rABV, and rATT were generated. A region of hypoperfusion due to AD was determined by statistical parametric mapping (SPM) analysis. Mean rCBF, rABV, and rATT values within the hypoperfused region were compared between the AD and control groups. RESULTS: Despite the significantly lower rCBF (P = .0004) in patients with AD (27.8 ± 7.1 mL/100 g/min) in comparison with control subjects (36.7 ± 6.3 mL/100 g/min), no significant difference in rATT was observed between the control (0.48 ± 0.09 seconds) and AD (0.47 ± 0.10 seconds) groups. Mean rABV was lower in the AD group (0.22 ± 0.10%) than in the control group (0.27 ± 0.12%), though the difference did not reach the level of statistical significance. CONCLUSIONS: Our results revealed that regional hypoperfusion in AD is not associated with rATT prolongation, suggesting that the mechanism of hypoperfusion is distinct from that in cerebrovascular diseases.

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