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Figure 1 Intriguingly, several key pathological features of PD align remarkably with the triggers and hallmarks of ferroptosis, including amplified lipid peroxidation, increased iron accumulation, suppressed expression of the cysteine-glutamate antiporter (system Xc - ) and diminished glutathione (GSH) levels ( SNCA triplication neurons is approximately 1.5-fold higher than that in control neurons, and exposure to 10 nM -syn oligomers further elevates lipid peroxidation levels ( Consequently, exploring ferroptosis as a pivotal mechanism in dopaminergic neuron demise offers promising avenues for novel therapeutic interventions in PD

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In secondary hypothyroidism the TSH is unreliable, and doses should be titrated to the T4 level Advise patients: Treatment is usually lifelong There is an association with other autoimmune diseases, particularly: Pernicious anaemia Addisons disease About the risk of side effects Typically few, and usually dose related due to too much thyroxine causing signs of hyperthyroidism: Palpitations and atrial fibrillation Diarrhoea Increase appetite Anxiety Insomnia Tremors Subclinical hypothyroidism Historically, a contentious issue Defined as elevated TSH, with normal T4