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Fig. 4 | Alzheimer's Research & Therapy

Fig. 4

From: Loss of perivascular aquaporin-4 localization impairs glymphatic exchange and promotes amyloid β plaque formation in mice

Fig. 4

Increased fine process AQP4 does not impair perivascular CSF-ISF exchange or alter amyloid β deposition. A Schematic outline of the workflow of the intracisternal tracer injection followed by the tracer visualization (left). Representative images of 70-kD CSF tracer distribution 90 min following injection are shown in animals 28 days after virus injection at right. Quantification of CSF tracer distribution showed that neither AQP4-M1 nor AQP4-M23 overexpression significantly altered 10 kD (B) or 70 kD (C) CSF tracer influx either into the whole brain, or into four subregions (cortex, hippocampus, striatum, and the diencephalon) compared to those injected with control virus. D Schematic outline of the workflow to define the effect of AQP4-M1 and AQP4-M23 overexpression on Aβ accumulation. Tg2576 mice at 3 months of age were injected with AAVPHP-M1, AAVPHP-M23, or null vector. Three months later, whole-brain human Aβ levels were assessed by ELISA. E At 6 months of age, no differences were observed in either hAβ1-40 or hAβ1-42 levels in either soluble or insoluble fractions from animals overexpressing AQP4-M1 or AQP4-M23 compared to null vector-injected controls

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