Current experimental evidence points to the conclusion that aquaporin 4 (AQP4), which is an important
water-channel membrane protein found in the brain, could play major roles in various brain conditions
pathologically including pathogenesis of Alzheimer's disease (AD). In this paper, we review how AQP4 and
altered astrocyte functions interact in AD, and provide experimental evidence highlighting the importance of this
topic for the future investigations. The interactions of AQP4 are as follows: (i) AQP4 could influence astrocytic
calcium signaling and potassium homeostasis. (ii) AQP4 is linked with the removal of interstitial β-amyloid and
glutamate transmission. (iii) Furthermore, AQP4 modulates the reactive astrogliosis and neuroinflammation
mechanisms. (iv) To add to this, AQP4 could participate in the AD pathogenesis through affecting neurotrophic
factor production. It is therefore possible to identify certain functional molecules that regulate astrocyte make-up
and functions. However, making crucial efforts to develop specific agents or drugs that target AQP4 function and
test their therapeutic efficiency will be a breakthrough for addressing AD in that AQP4 controls the various
physiological as well as pathophysiological features of astrocytes.
Keywords: Alzheimer's disease, astrocytes, cerebrospinal fluid, glutamate transmission, glymphatic system, aquaporin 4.
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