Early Alzheimer’s and Parkinson’s Disease Pathology in Urban Children: Friend versus Foe Responses—It Is Time to Face the Evidence
Figure 4
(a) Eleven year MCMA girl dorsal motor nucleus of the vagus stained with anti-8-OHdG showing immunohistochemical staining of oxidized nucleoside in neurons. 8-hydroxyguanosine is a modified base that occurs in DNA due to attack by hydroxyl radicals that are formed as byproducts and intermediates of aerobic metabolism and during oxidative stress. 8-OHdG immunohistochemistry red product. (b) Same 11 y old girl as in Figure 4(a) showing caudal pontine reticular nucleus neuronal protein oxidation marked by nitrotyrosine immunoreactivity. (c) Frontal cortex in an APOE 3/3 17 y old MCMA teen. A diffuse amyloid plaque (red product) is seen surrounded by glial cells negative for reactive astrocytes as detected by their reaction to the glial fibrillary acidic protein (GFAP). Dual immunohistochemistry for amyloid beta 1–42 and GFAP (DAB + brown product). (d) Frontal cortex in a 36 y old MCMA male APOE 3/4. This subject shows numerous diffuse and mature amyloid beta 1–42 plaques. (e) Frontal cortex in a 15 y old MCMA APOE 3/3 boy. Abnormal tau protein positive with the Tau 8 antibody (Innogenetics, Belgium), both in the neuronal body and in neuritis. (f) Frontal cortex in a 15 y old MCMA APOE 3/4 boy. A clear Tau 8 positive neurite is seen.
