Mitochondria are the proximate target of a number of different neurotoxins. Typically, impairing of the key bioenergetic function of mitochondria by toxins is considered as the main mechanism of action. However, the effective maintenance of energy generation in neurons depends on the biogenesis, trafficking, and degradation of mitochondria in addition to the traditional bioenergetic functions. We have recently demonstrated that glutamate alters both the trafficking and morphology of mitochondria in primary neurons. In addition, several other potential neurotoxins, including nitric oxide and zinc, inhibit mitochondrial movement and, in some cases, alter morphology too. This suggests that some part of the action of neurotoxins might include the impairment of mitochondrial trafficking in neurons, with the resultant failure of local ATP delivery.
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- Research indicates that mutated tau proteins can inhibit this process, affecting cell health during oxidative stress.
- In this study, it was found that certain tau mutations reduce levels of a key mitophagy receptor, FKBP8, which could help explain tau's role in mitochondrial dysfunction related to Alzheimer's and suggest FKBP8 as a target for future treatments.
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