Cerebral hemodynamics and capillary dysfunction in late-onset major depressive disorder
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Cerebral hemodynamics and capillary dysfunction in late-onset major depressive disorder. / Dalby, Rikke B.; Eskildsen, Simon F.; Videbech, Poul; Rosenberg, Raben; Østergaard, Leif.
I: Psychiatry Research - Neuroimaging, Bind 317, 111383, 2021, s. 1-10.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Cerebral hemodynamics and capillary dysfunction in late-onset major depressive disorder
AU - Dalby, Rikke B.
AU - Eskildsen, Simon F.
AU - Videbech, Poul
AU - Rosenberg, Raben
AU - Østergaard, Leif
N1 - Publisher Copyright: © 2021
PY - 2021
Y1 - 2021
N2 - In major depressive disorder (MDD), perfusion changes in cortico-limbic pathways are interpreted as altered neuronal activity, but they could also signify changes in neurovascular coupling due to altered capillary function. To examine capillary function in late-onset MDD, 22 patients and 22 age- and gender-matched controls underwent perfusion MRI. We measured normalized cerebral blood flow (nCBF), cerebral blood volume (nCBV), and relative transit-time heterogeneity (RTH). Resulting brain oxygenation was estimated in terms of oxygen tension and normalized metabolic rate of oxygen (nCMRO2). Patients revealed signs of capillary dysfunction (elevated RTH) in the anterior prefrontal cortex and ventral anterior cingulate cortex bilaterally and in the left insulate cortex compared to controls, bilateral hypometabolism (parallel reductions of nCBV, nCBF, and CMRO2) but preserved capillary function in the subthalamic nucleus and globus pallidus bilaterally, and hyperactivity with preserved capillary function (increased nCBF) in the cerebellum and brainstem. Our data support that perfusion changes in deep nuclei and cerebellum reflect abnormally low and high activity, respectively, in MDD patients, but suggest that microvascular pathology affects neurovascular coupling in ventral circuits. We speculate that microvascular pathology is important for our understanding of etiology of late-onset MDD as well as infererences about resulting brain activity changes.
AB - In major depressive disorder (MDD), perfusion changes in cortico-limbic pathways are interpreted as altered neuronal activity, but they could also signify changes in neurovascular coupling due to altered capillary function. To examine capillary function in late-onset MDD, 22 patients and 22 age- and gender-matched controls underwent perfusion MRI. We measured normalized cerebral blood flow (nCBF), cerebral blood volume (nCBV), and relative transit-time heterogeneity (RTH). Resulting brain oxygenation was estimated in terms of oxygen tension and normalized metabolic rate of oxygen (nCMRO2). Patients revealed signs of capillary dysfunction (elevated RTH) in the anterior prefrontal cortex and ventral anterior cingulate cortex bilaterally and in the left insulate cortex compared to controls, bilateral hypometabolism (parallel reductions of nCBV, nCBF, and CMRO2) but preserved capillary function in the subthalamic nucleus and globus pallidus bilaterally, and hyperactivity with preserved capillary function (increased nCBF) in the cerebellum and brainstem. Our data support that perfusion changes in deep nuclei and cerebellum reflect abnormally low and high activity, respectively, in MDD patients, but suggest that microvascular pathology affects neurovascular coupling in ventral circuits. We speculate that microvascular pathology is important for our understanding of etiology of late-onset MDD as well as infererences about resulting brain activity changes.
KW - Capillary dysfunction
KW - Capillary transit time heterogeneity (CTH)
KW - Cerebral blood flow (CBF)
KW - Cerebral blood volume (CBV)
KW - Default mode network (DMN)
KW - Magnetic resonance imaging (MRI)
KW - Major depressive disorder (MDD)
KW - Neurovascular coupling
KW - Relative transit time heterogeneity (RTH)
UR - http://www.scopus.com/inward/record.url?scp=85114612404&partnerID=8YFLogxK
U2 - 10.1016/j.pscychresns.2021.111383
DO - 10.1016/j.pscychresns.2021.111383
M3 - Journal article
C2 - 34508953
AN - SCOPUS:85114612404
VL - 317
SP - 1
EP - 10
JO - Psychiatry Research: Neuroimaging
JF - Psychiatry Research: Neuroimaging
SN - 0925-4927
M1 - 111383
ER -
ID: 304369692