Front aging neurosci: interaction of autophagy with NLRP3 inflammasomes in Alzheimer's and Parkinson's diseases

Autophagy is a standard and tightly regulated cellular self-degradation process responsible for engulfing damaged organelles, misfolded proteins, and pathogens that invade the bilayer membrane called autophagosomes and guide them to lysosomal degradation, which plays a vital role
in metabolism and energy balance in the body.

Studies have found that when autophagy changes, abnormal accumulation of damaged organelles and abnormally folded proteins within cells can lead to irreversible damage
.
Numerous studies confirm that autophagy and pathological proteins interact
in the development of neurodegenerative diseases.
In most autophagy lysosomal diseases, the brain tends to be the most affected organ, and neurons rely heavily on autophagy to maintain normal function and homeostasis, suggesting that autophagy plays a vital role
in neuronal health.
To date, autophagy has been shown to induce neurodegeneration and exacerbate disease progression
.
However, the specific mechanism of autophagy in the development of neurodegenerative diseases remains unclear
.
Therefore, it is necessary to further explore the regulatory role
of autophagy in neurodegenerative diseases within the scope of physiological relevance.
The purpose of this review is to review recent studies on the interaction between autophagy, NLRP3 inflammasomes and protein aggregates in Alzheimer's disease (AD) and Parkinson's disease (PD), analyze their mechanism of action, and provide theoretical reference
for further research.