Early disrupted neurovascular coupling and changed event level hemodynamic response function in type 2 diabetes: an fMRI study

João V. Duarte, João M. S. Pereira, Bruno Quendera, Miguel Raimundo, Carolina Moreno, Leonor Gomes, Francisco Carrilho, Miguel Castelo-Branco*

*Autor correspondente para este trabalho

Resultado de pesquisarevisão de pares

53 Citações (Scopus)


Type 2 diabetes (T2DM) patients develop vascular complications and have increased risk for neurophysiological impairment. Vascular pathophysiology may alter the blood flow regulation in cerebral microvasculature, affecting neurovascular coupling. Reduced fMRI signal can result from decreased neuronal activation or disrupted neurovascular coupling. The uncertainty about pathophysiological mechanisms (neurodegenerative, vascular, or both) underlying brain function impairments remains. In this cross-sectional study, we investigated if the hemodynamic response function (HRF) in lesion-free brains of patients is altered by measuring BOLD (Blood Oxygenation Level-Dependent) response to visual motion stimuli. We used a standard block design to examine the BOLD response and an event-related deconvolution approach. Importantly, the latter allowed for the first time to directly extract the true shape of HRF without any assumption and probe neurovascular coupling, using performance-matched stimuli. We discovered a change in HRF in early stages of diabetes. T2DM patients show significantly different fMRI response profiles. Our visual paradigm therefore demonstrated impaired neurovascular coupling in intact brain tissue. This implies that functional studies in T2DM require the definition of HRF, only achievable with deconvolution in event-related experiments. Further investigation of the mechanisms underlying impaired neurovascular coupling is needed to understand and potentially prevent the progression of brain function decrements in diabetes.

Idioma originalEnglish
Páginas (de-até)1671-1680
Número de páginas10
RevistaJournal of Cerebral Blood Flow and Metabolism
Número de emissão10
Estado da publicaçãoPublicado - 3 out. 2015
Publicado externamenteSim

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