Glycolysis: The Bridge Between Cellular Interaction and Alzheimer's Disease.

The pathological progression of Alzheimer's disease (AD) involves not only intrinsic neuronal lesions but is also closely associated with dysregulation of intercellular communication within the neuroimmune microenvironment. Glycolysis, as a central pathway in cellular energy metabolism, exhibits significant abnormalities in AD, and changes in its activity may further influence disease progression by modulating interactions between neurons. This article aims to systematically elucidate how glycolysis, as a key component of metabolic regulation, participates in the regulation of cellular interactions during the progression of AD, and to explore its potential mechanisms and therapeutic implications. Firstly, it systematically reviews the key changes in interactions between cells in AD, including microglia, astrocytes, oligodendrocytes, and neurons, and their roles in neuroinflammation, synaptic loss, and amyloid deposition. Secondly, by analysing alterations in the glycolytic metabolic profiles of various neuronal cell types in AD, we explore in depth how glycolysis regulates cellular signalling, inflammatory responses, and cellular function, thereby influencing cell-cell interactions. Lastly, by combining current research on the control of the glycolytic pathway in AD with possible therapeutic methods, we propose a novel way to stop the progression of the disease by focusing on cell interactions through mediating glycolysis. By tracing the causal chain in AD through which glycolysis acts as a bridge via altered cell-cell interactions, this paper aims to provide a theoretical basis for the development of disease-modifying therapies based on metabolic reprogramming.