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Alzheimer’s disease (AD) is the most prevalent cause of dementia. Among many of its hallmarks, tauopathies represent an emerging nosographic concept that could explain the mechanism by which neurodegeneration progresses in brain regions, culminating in cognitive dysfunction. AD is the ultimate outcome of a complex multifactorial neurodegenerative process in which distinct neurobiological mechanisms operate from early to late stages of the disease. AD pathology is characterized by the well-known presence of amyloid plaques in the cortex and hippocampal formation, hyperphosphorylated forms of microtubule-associated protein tau, neurofibrillary tangles, and synaptic pathology. Starting from the early stages, the disease is associated with neurodegeneration in specific brain regions. The convergence of amyloid and tau on cognitive impairment has been widely investigated, but the relative contribution of each cause to cognitive dysfunctions remains undetermined. The involvement of tau-related processes in the neuronal and synaptic dysfunction might represent a common mechanism at play at early stages. Tauopathy disrupts the structure and function of synapses and inhibits long-term potentiation, and can promote or counteract amyloid toxicity. Abnormal tau phosphorylation leads to its hyperphosphorylation, misfolding, aggregation, and intracellular neuronal distribution, which can underlie synaptic dysfunction, leading to memory loss. Pathological tau becomes toxic at later stages of the disease, and cellular stress might intensify the aberrant phosphorylation of tau, resulting in the release of its toxic fragments. Accumulation of insoluble aggregates of toxic tau species in the soma and nuclei makes neurons unresponsive to neuronal activity, weakening the integrity of neuronal networks and leading to the loss of cognitive functions. Since tau is a microtubule-associated protein, its increase in aggregation and accumulation may affect the integrity of axons and dendrites. Moreover, recent evidence suggests that tau expression could have a neuroprotective role in early stages of the disease. However, chronic tau
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