Multiple sources of iron may be relevant to amyloid–iron interaction in AD such as: ferritin-bound ferrihydrite, transferrin, labile iron pools (including jettisoned ferritin iron content75), hemosiderin formed at sites of microbleeds and haemorrhage in the brain, from disrupted neuronal mitochondria, and/or potential external sources of iron such as airborne particulate matter which have been suggested to enter the brain via the olfactory bulb.76 Furthermore, the influence of the initial iron phase upon amyloid's reductant properties in vivo has not previously been characterised. The gene discussed is TF; the disease is Alzheimer disease.