Cell Death Differ: The absence of TfR2 in Parkinson's models has a neuropersonal protective effect

Parkinson's disease (PD) is a neurodegenerative disease that mainly affects dopamine energy (DA) neurons in the black synth circuit of the basal nerve section.
the disease is iditable, with less than 10% of cases attributable to single-gene causes.
complex causes of PD, involving complex gene-environment interactions, the main risk factor is aging.
mitochondrial dysfunction, the aggregation of α-synaptic nucleoproteins, and the subsequent protein toxicity stress and harmful oxidative stress response have been identified as the main pathogenic mechanisms of the disease.
PD is still difficult to treat, it is particularly important to identify specific path paths that can target the development of disease.
the disorder of iron metabolism occurs in both idynapathic and hereditary PD, accompanied by the deposition of iron in the dark denser part (SNpc) and its DA neurons.
these changes or have far-reaching neuropathological implications.
of iron also changes in aging, a major risk factor for PD.
TfR2 deficiency has a protective effect on mice treated with 52-week-old mptp, reducing iron load by chelation has been considered a viable treatment strategy for disease improvement.
, iron chelation strategies are still imperfect due to widespread adverse side effects and lack of specificity.
therefore, a more effective approach is to look for specific signaling path paths associated with iron overload in PD-related brain regions, especially in black-related brain regions.
Previous studies have shown that the iron transport mechanism of TfR2 (translatin/translatin-2) plays a crucial role in melanin dopamine neurons, which is disrupted in PD models and patients and may therefore be a potential therapeutic target to prevent iron deposition.
the effect of Tfr2 targeting loss on PD models in order to verify this hypothesis, the study constructed a mouse model of dopamine-energy neurons targeting and knocking out TfR2.
the model, the researchers modeled PD in a variety of ways based on the exposure of neurotoxins or the protein toxicity mechanisms of α-synaptic nucleoproteins.
researchers have found that the absence of TfR2 can act as a nerve protection by fighting dopamine neuron degeneration, PD, and iron overload associated with aging.
further studies have found that the effect is more pronounced in women than in men.
, the results suggest that the iron transport effect of TfR2 may be a strategy to deter the development of PD.
, however, the findings also suggest that treatment strategies for TfR2 should consider the potential gender-secondary nature of neuropne protection reactions.
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