Alzheimer's disease (AD) is a common neurodegenerative disorder nowadays. Amyloid-beta (Aβ) and tau proteins are among the main contributor to the development or propagation of AD. In AD, Aβ proteins clump together to form plaques and disrupt cell functions. On the other hand, the abnormal chemical change in the brain helps to build sticky tau tangles that block the neuron's transport system. Astrocytes generally maintain a healthy balance in the brain by clearing the Aβ plaques (toxic Aβ). But, over-activated astrocytes release chemokines and cytokines in the presence of Aβ and also react to pro-inflammatory cytokines further increasing the production of Aβ. In this paper, we construct a mathematical model that can capture astrocytes' dual behaviour. Furthermore, we reveal that the disease propagation does not depend only on the current time instance; rather, it depends on the disease's earlier status, called the "memory effect". We consider a fractional order network mathematical model to capture the influence of such memory effect on AD propagation. We have integrated brain connectome data in the network model and studied the memory effect and the dual role of astrocytes together. Depending on toxic loads in the brain, we have also analyzed the neuronal damage in the brain. Based on the pathology, primary, secondary, and mixed tauopathies parameters have been used in the model. Due to the mixed tauopathy, different brain nodes or regions in the brain connectome accumulate different toxic concentrations of toxic Aβ and toxic tau proteins. Finally, we explain how the memory effect can slow down the propagation of such toxic proteins in the brain and hence decreases the rate of neuronal damage.