The complement system comprises intrinsic complement components,complement regulatory pro-teins,and complement receptors.Complement activation plays a role in promoting the sensitization of peripheral pain re-ceptors,enhancing immune cell activity,and participating in the regulation of axon regeneration after nerve injury.The in-teraction of the complement system contributes to the development and maintenance of pathological pain,affecting the dor-sal root ganglion neurons,spinal dorsal horn,and brain.Consequently,targeting the complement system holds promise as a therapeutic approach for neuropathic pain treatment.This paper reviews the progress in understanding the functions of the complement system and its implications in pathological pain,offering valuable insights for the future development of targeted drug therapies.

Alzheimer's disease(AD)is a common neurological degenerative disease.Collapsin response mediator protein2(CRMP2)plays an important role in the progression of AD.Hyperphosphorylation of CRMP2 results in decreased stability of axonal terminal microtubules and abnormal axoplasmic transport of neurons,which leads to abnormal mitochondrial dynamics of neurons,inhibits the ability of lysosomal autophagy,and leads to excessive activation of NMDA receptors.The phosphorylation of CRMP2 provides a new idea for AD drug develop-ment.In this review,the molecular mechanisms of CRMP2 involved in AD are reviewed,which can provide refer-ences for the development of targeted drugs.

Alzheimer's disease(AD)is a common neurodegenerative disease,which is mainly caused by brain lesions.The activation of complement system plays an important role in the process of AD lesions.The activated complement can bind to cell membrane receptors and regulate downstream signals.Therefore,inhibiting complement activation provides a new idea for AD treatment.This article reviews the progress in the mechanism and drug development of complement activation in AD,which may provide a new perspective for the diagnosis,treatment and drug development of AD.