Abstract

The current study reviews computational models that embody a hypothesis and/or a theory of mechanisms of how AD impacts the brain and cognition as well as provide a critical analysis of strengths and weaknesses of these models. Existing models assume AD symptoms stem from abnormalities to cell structure, synaptic connections, neuro-chemicals, as well as other neural circuits and systems. We also discuss how mathematical formulation of the known biology of AD can help us understand AD symptoms and how pharmacological medications and neurostimulation therapies may work. Finally, we discuss general research directions that may improve future treatments of the disease.