Editorial on the Research Topic Molecular mechanisms of Alzheimer's disease: From top to bottom Alzheimer's disease (AD) is a neurodegenerative disease related to aging. It is a type of senile dementia of high prevalence worldwide. It causes a gradual increase in irreversible cognitive decline that includes memory deficits, behavioral alterations and mental confusion, triggering devasting effects on daily life.In AD, the damage and destruction of neurons gradually affect different parts of the brain. Neurodegeneration is preceded by the deposition of soluble oligomers and fibrils of the amyloid-β (Aβ) peptide in the extracellular space and by intracellular aggregation of the tau protein in neurofibrillary tangles (Pratico, 2008;Paula-Lima et al., 2013). According to the amyloid cascade, the accumulation of the extracellular Aβ peptide triggers the dysfunction in the release of neurotransmitters, extensive oxidative stress (Butterfield and Lauderback, 2002;Ill-Raga et al., 2010), synaptic failure and neuronal loss, leading to macroscopic atrophy (Lane et al., 2015).Genetic and environmental factors are related to the risk of AD. Although current pharmacological treatments offer some relief from AD symptoms, the improvement is modest and temporary, indicating that the heterogeneity of the disease requires a stratified approach for effective treatment (Conway, 2020). Some non-pharmacological interventions have been investigated and show promissory effects. Between them, we highlighted the different types of physical exercise, which act by multiple neuroprotective mechanisms (Daré et al., 2020;Soares et al., 2021). However, until now, there is no curative treatment for AD, and researchers are still struggling to find therapeutic targets that promote significant improvements in the clinical conditions of Alzheimer's patients (Knopman et al., 2021). In this context,