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Yuki Mori

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YNIMG Journal 2026 Journal Article

Unmasking the bias: Can diffusion-weighted imaging reliably assess glymphatic function in awake and anesthetized brain?

  • Ryszard Stefan Gomolka
  • Antonio Ladrón-de-Guevara
  • Søren Grubb
  • Lydiane Hirschler
  • Isabelle Strom
  • Pia Weikop
  • Matthias van Osch
  • Maiken Nedergaard

This study investigated whether magnetic resonance (MR) diffusivity parameters derived from diffusion-weighted imaging (DWI) can serve as biomarkers of glymphatic function in awake and anesthetized mice. Spectral apparent diffusion coefficient (ADC) analysis, obtained using an inverse Laplace transform, revealed that both Isoflurane (ISO) and Ketamine/Xylazine (K/X) anesthesia reduced the magnitude and range of diffusivities associated with interstitial fluid space (≤1 µm²/ms) compared with the awake state. Perfusion-related diffusivities (20-80 µm²/ms) increased under ISO but decreased under K/X. Monoexponential ADC and biexponential intravoxel incoherent motion (IVIM) modeling showed that ISO dose-dependently elevated, while K/X reduced, both slow and fast diffusivities across the brain. Dynamic contrast-enhanced MRI (DCE-MRI) indicated intermediate glymphatic influx in awake mice relative to both anesthetic conditions, without regional correlation to DWI-derived parameters. Perfusion micro-computed tomography (µCT) further demonstrated that ADC and IVIM metrics correlated regionally with mean transit time, suggesting a confounding by cerebral blood flow (CBF). Two-photon microscopy confirmed anesthesia-induced changes in cortical microvessel diameters consistent with perfusion alterations. Collectively, these findings indicate that MR diffusivity measures are strongly influenced by state-dependent physiological changes, and in particular perfusion. This represents an important limitation that warrants caution when using DWI to compare extracellular space, interstitial fluid flow, or glymphatic activity across different physiological or anesthetic states. Therefore, although technically challenging, we suggest that DWI studies aimed at assessing glymphatic or interstitial dynamics should be performed in awake conditions to minimize variability and anesthesia-related perfusion confounds across studies.

Details DOI

YNICL Journal 2018 Journal Article

Inflammatory projections after focal brain injury trigger neuronal network disruption: An 18F-DPA714 PET study in mice

  • Sanae Hosomi
  • Tadashi Watabe
  • Yuki Mori
  • Yoshihisa Koyama
  • Soichiro Adachi
  • Namiko Hoshi
  • Mitsuo Ohnishi
  • Hiroshi Ogura

Due to the heterogeneous pathology of traumatic brain injury (TBI), the exact mechanism of how initial brain damage leads to chronic inflammation and its effects on the whole brain remain unclear. Here, we report on long-term neuroinflammation, remote from the initial injury site, even after subsiding of the original inflammatory response, in a focal TBI mouse model. The use of translocator protein-positron emission tomography in conjunction with specialised magnetic resonance imaging modalities enabled us to visualize "previously undetected areas" of spreading inflammation after focal cortical injury. These clinically available modalities further revealed the pathophysiology of thalamic neuronal degeneration occurring as resident microglia sense damage to corticothalamic neuronal tracts and become activated. The resulting microglial activation plays a major role in prolonged inflammatory processes, which are deleterious to the thalamic network. In light of the association of this mechanism with neuronal tracts, we propose it can be termed "brain injury related inflammatory projection". Our findings on multiple spatial and temporal scales provide insight into the chronic inflammation present in neurodegenerative diseases after TBI.

Details DOI
v2026.09.13