Neurovascular Coupling in Type 2 Diabetes With Cognitive Decline. A Narrative Review of Neuroimaging Findings and Their Pathophysiological Implications

Figures

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  Figure 1. Overview of the complex and multifactorial mechanisms which lead to impaired cognition in type 2 diabetes. The focus of this review is the specific diabetic influence on neurovascular coupling and how this leads to impaired cognition (bold in the figure).

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  Figure 2. Possible scenario for clinical progression (x-axis) from pre-diabetes to manifest clinical diabetic “cognopathy”. Moderators and comorbidity represent all diseases and factors present before and after T2DM onset such as sleep apnea, obesity, hypertension etc. Adapted from Jessen and colleagues (27).

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  Figure 3. Schematic summary of the neurovascular coupling cascade (46). The cellular substrate for each step is seen, PN – principal neuron, IN – interneuron, AC – astrocyte, PC – pericyte, SMC – smooth muscle cell, ETC – endothelial cells, SC-proj. – subcortical projections from locus coeruleus, basal forebrain, raphe nuclei, PV-proj. – perivascular projections from cranial autonomic ganglia. The bottom rows describe the possible influence of diabetes on each step and how this has been detected.

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  Figure 4. Idealized BOLD response. Steady-state is disrupted by a stimulus which results in an initial dip, an overshoot and lastly an undershoot before steady-state is re-acquired. The rising curve reflects an increase in magnetic field uniformity due to washout of paramagnetic deoxyhemoglobin.