Topic: mitochondrial fission

Brain-Derived Neurotrophic Factor (BDNF) is an important regulator of synaptic activity and a mediator of LTP of hippocampal synapses. Furthermore, synaptic activity controls mitochondrial fission and dynamic control of fission regulates plasticity induction in hippocampus. Given the important role of mitochondrial fission in establishing LTP and knowing the key role of BDNF in LTP induction, we hypothesized that the effects of BDNF on synaptic potentiation could be mediated by mitochondrial fission. We observed that local protein synthesis of Drp1, a key mediator of mitochondrial fission, is

Cellular hallmarks of neurodegenerative diseases include loss of synapses, neuronal death, inflammation, energy homeostasis defects, oxidative stress, mitochondrial dysfunction, and aberrant proteostasis. AMP-activated kinase (AMPK) maintains energy homeostasis by responding to fluctuating ATP levels, with diverse targets ranging from changing the transcriptional program, promoting glucose uptake, inhibiting protein synthesis, inducing mitochondrial fission, mitophagy and autophagy. Evidence indicates that AMPK is hyperactivated in Alzheimer’s disease (AD), and amyloid-β (Aβ) can activate AMPK

Following injury, astrocytes undergo major alterations in morphology and gene expression, leading to the acquisition of distinct “reactivity” states that play important roles in brain tissue repair. Evidence indicates that these cellular states are also marked by rewiring of mitochondrial energy metabolism, i.e. the central hub for cellular energy metabolism and metabolic signaling. However, how such mitochondrial responses are regulated and how they may influence astrocyte reactivity remains unclear. Our prior research unveiled temporal and region-specific morphological changes in astrocytic

Alterations along the brain-gut axis participate in the pathogenesis of neurodegenerative diseases. Recent data suggest that the gut microbiota partially exerts its action by modulating neuroinflammation. Interestingly, neuroinflammation has been postulated as one of the leading causes of Alzheimer’s Disease (AD). Therefore, targeting brain inflammation has been suggested as a promising therapeutic strategy to cope with AD. In this regard, neuroinflammation has been related to the soluble epoxide hydrolase (sEH) enzyme, which is upregulated in the brains of AD patients and mice models of AD. C

Neurogenesis is the process by which dividing neural stem/progenitor cells (NSPCs) produce post-mitotic cells. The balance between self-renewal and differentiation is a highly controlled process under the influence of intrinsic and extrinsic factors. Previous studies have pointed to a model whereby cell fate is largely determined before the last mitosis. However, recent findings indicate that in the cerebral cortex mitochondrial dynamics have an impact on neurogenesis after the last cell division. Daughter cells with high levels of mitochondrial fusion undergo self-renewal, whereas those cells