Dementia from Small Vessel Disease Versus Alzheimer’s Disease: Separate Diseases or Distinct Manifestations of Cerebral Capillopathy Due to Blood–Brain Barrier Dysfunction? A Pilot Study

Figures

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  Figure 4. Late phase glymphatic slopes for AD, SVD, and control subjects by region. Significant differences in glymphatic clearance slopes are noted when comparing SVD and AD slopes with the controls. There are no regions where the SVD and AD groups are significantly different from one another.

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  Figure 5. Arterial phase peak amplitude for AD, SVD, and control subjects by region. Here, AD and SVD subjects were compared to each other and to controls, including data limited to each specific region with reduced glymphatic clearance. No significant differences between the groups AD, SVD, and controls were noted. Thus, the arterial phase amplitudes were unimpaired.

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  Figure 6. Arterial phase peak latency for AD, SVD, and control subjects by region. Here, for AD and SVD subjects, the included data have been limited to each specific region with reduced glymphatic clearance. No significant differences between SVD and AD, or when either group is compared to controls in the arterial phase in brain regions demonstrating significant reduction in glymphatic phase clearance. The arterial phase peak latency was unimpaired in those regions.

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  Figure 7. Cerebral capillopathy schematic leading to Alzheimer’s dementia, including risk factors, initial target (BBB dysfunction with leak), producing vascular injury, and metabolic consequences. Accelerating factors that further capillary dysfunction include accumulating misfolded proteins, capillary loss, and genetic factors (GF). The rate of cognitive decline increased by GF, reducing the normal handling of misfolded proteins.

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  Figure 1. Perfusion cycle with arterial, venous, and capillary components versus time. The 5-arterial phase PLD times are illustrated by the orange line (800–1200 ms, 200 ms intervals), the 7-capillary phase PLD’s (2800–4000 ms at 200 ms intervals) by the red line. T1 times (63% signal decay) of major tissue signal contributors are indicated by the colored dots. Magenta dot = 800–850 ms T1 of white matter. Orange dot = 1650 ms T1 of blood. Green dot = 1700 ms T1 of gray matter (all values are for 3T). Dk blue dot = 3800 ms T1 of water (CSF fluid); (all values are for 3T). BAT = bolus arrival time; aaTT =artery-artery arrival time; τ = peak capillary arrival time. Adapted with publisher permission (Wiley) from [33].

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  Figure 2. Early phase arterial peak amplitude for AD, SVD, and control subjects by region. AD = Alzheimer’s Disease, SVD = small vessel disease, L/RTEMP = Left/Right temporal lobe, L/RFRONT = L/R Frontal lobe, L/RPAR = L/R Parietal lobe. There were no significant statistical differences among the three groups. The box =interquartile range (IQR) 25 (1st) to 75 (3rd) percentile; whisker = 1st IQR − 1.5 X1st IQR and 3rd IQR + 1.5X 3rd IQR. Black dots = outliers in line with their respective group. This applies to Figure 3, Figure 4, Figure 5 and Figure 6.

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  Figure 3. Early phase arterial peak latency for AD, SVD, and control subjects by region. There were no significant statistical differences among the three groups.

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  Figure 8. Note the locations of the Region of Interest drawn for each anatomic location (shown as blue ellipses unilaterally for clarity). Temporal lobe volume = 650 mm2, Frontal lobe = 1150 mm2, Parietal lobe = 760 mm2.