. Dysregulation of Neuronal Iron Homeostasis as an Alternative Unifying Effect of Mutations Causing Familial Alzheimer's Disease. Front Neurosci. 2018;12:533. Epub 2018 Aug 13 PubMed.

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  1. This is a well-thought-out hypothesis paper. It presents us with a new intellectual framework for future studies of the role of familial Alzheimer’s disease mutations in the amyloid precursor protein (APP) and presenilin genes to change iron, metal, and oxidative homeostasis in neurons. 

    Previously, the scientific and medical communities had been completely focused, for good reason, on the capacity of key familial AD mutations to act to change the cleavage rate of the APP protein to generate amyloid. It should be noted, however, that amyloidosis is not present in all patients with AD-like cognitive change and that papers in excellent journals since 2000, along with other recent publications (Venkataramani et al., 2018; Belaidi et al., 2018) support APP’s role in oxidative iron homeostasis. This present publication gives impetus for future studies of APP's biological function in iron/metal homeostasis, for example, in children and adults long before the onset of amyloidosis and senility.

    References:

    . Manganese causes neurotoxic iron accumulation via translational repression of Amyloid Precursor Protein (APP) and H-Ferritin. J Neurochem. 2018 Aug 27; PubMed.

    . Marked Age-Related Changes in Brain Iron Homeostasis in Amyloid Protein Precursor Knockout Mice. Neurotherapeutics. 2018 Aug 15; PubMed.

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