Stress damages the brain and is a risk factor for Alzheimer’s disease. Alzheimer’s disease is a progressive neurodegenerative diseases that is associated with the abnormal upregulation of oxidative stress, and its pathology is characterized by deposition of extracellular β-amyloid (Aβ) plaques and intracellular neurofibrillary tangles. Mitochondrial dysfunction and synaptic dysfunctions are early pathological features of Alzheimer’s disease-affected brains. Mitochondria are a major source of reactive oxygen species (ROS), and mitochondria-mediated oxidative stress contributes to Aβ and tau oligomer formation and accumulation. Therefore, inhibiting mitochondrial oxidative stress and dysfunctions could be a promising therapeutic target to prevent and treat Alzheimer’s disease.

Specific aims of the issue of Stress and Alzheimer's disease are to explore:

The proposed journal will encompass a wide range of articles, including original research, review papers, case studies, and expert commentaries, all focused on various aspects of laboratory medical education. The journal may include topics related to:

(1) Regulation of stress to Aβ formation and tau phosphorylation and oligomerization;

(2) Relationship between stress and mitochondrial defects during Alzheimer’s disease;

(3) Contribution of stress to synaptic function and neurodegeneration induced memory deficiency during Alzheimer’s disease;

(4) Effect of stress-targeted compounds or drugs on the progression and neurodegeneration of Alzheimer’s disease.

We invite researchers, educators and practitioners to contribute their insights, experiences and research findings to this special issue.