Mitochondrial dysfunction and Alzheimer's disease: pathogenesis of mitochondrial transfer

Abstract

In recent years, mitochondrial transfer has emerged as a universal phenomenon intertwined with various systemic physiological and pathological processes. Alzheimer's disease (AD) is a multifactorial disease, with mitochondrial dysfunction at its core. Although numerous studies have found evidence of mitochondrial transfer in AD models, the precise mechanisms remain unclear. Recent studies have revealed the dynamic transfer of mitochondria in Alzheimer's disease, not only between nerve cells and glial cells, but also between nerve cells and glial cells. In this review, we explore the pathways and mechanisms of mitochondrial transfer in Alzheimer's disease and how these transfer activities contribute to disease progression.

Keywords: AD treatment; Alzheimer’s disease; mitochondrial dysfunction; mitochondrial transfer; neuroprotection.

Figure 1

Mitochondrial dysfunction and pathological features form a vicious cycle in AD pathology. Aβ accumulation, Tau hyperphosphorylation, or Aβ-Tau interaction can all contribute to mitochondrial dysfunction, which in turn exacerbates abnormalities in all three, which further impair mitochondrial function.

Figure 2

Anterograde and retrograde directions of intracellular mitochondrial movement. In this process, kinesin is responsible for moving mitochondria in an anterograde direction toward the nerve terminal, whereas kinesin and dynein move mitochondria in a retrograde direction toward the soma.