Alzheimer’s disease is the most common neurodegenerative disorder resulting in dementia in the elderly. Clinically, it consists in acquired progressive behavioural changes and cognitive decline, while pathologically it is characterised by synaptic and neuronal loss. Senile plaques, which consist in aberrant extracellular accumulation of amyloid peptides, and neurofibrillary tangles, which consist equally in aberrant, but in this case intracellular accumulation of hyperphosphorylated tau, represent the pathological hallmarks of Alzheimer’s disease. Intriguingly, senile plaques and neurofibrillary tangles, are both linked to axonal pathology and impairments in axonal transport. Microtubule-dependent axonal transport can be divided into anterograde and retrograde with mechanisms of its regulation and its role in Alzheimer’s disease still to be elucidated. This is true also for the basic mechanisms underlying axonal pathology formation in Alzheimer’s disease in beyond.
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