Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a gradual onset and progression, primarily affecting individuals aged 65 and older.

The incidence of AD doubles every five years after the age of 65, with a prevalence rate reaching 50% in those over 85.

Research indicates that neuronal aging plays a significant role in cognitive decline associated with AD, as aging neurons often contain Tau neurofibrillary tangles, a hallmark of the disease.

The complex pathogenesis of Alzheimer's disease is multifactorial, involving genetics, environmental influences, and lifestyle factors.

Current studies focus on key mechanisms such as the amyloid beta (Aβ) cascade hypothesis, Tau protein phosphorylation, oxidative stress, and neuroinflammation in relation to neuronal senescence and AD.

Aging neurons contribute to AD through various mechanisms, including the accumulation of amyloid beta, abnormal Tau phosphorylation, oxidative stress, inflammatory responses, and damage to the cholinergic system.

With age, neurons experience reduced glucose metabolism efficiency, which increases their vulnerability to toxic damage and negatively impacts cognitive function.

Emerging anti-neuronal aging therapies are being recognized as crucial strategies in the treatment of Alzheimer's disease.

Research reviews are exploring treatment methods that specifically target neuronal aging, aiming to provide new therapeutic options for Alzheimer's disease.

This research is supported by the National Natural Science Foundation of China and declares no conflicts of interest.