Increased monoamine oxidase b activity in plaque-associated astrocytes of Alzheimer brains revealed by quantitative enzyme radioautography

Evidence for Astrocytosis in Prodromal Alzheimer Disease Provided by 11C-Deuterium-L-Deprenyl: A Multitracer PET Paradigm Combining 11C-Pittsburgh Compound B and 18F-FDG

“…The late 40-to 60-min 11 C-PIB sum image was created and used for subsequent image analysis. For each 18 F-FDG acquisition, 21 frames (4 · 30, 9 · 60, 3 · 180, and 5 · 300 s) were acquired over 45 min. A late 25-to 45-min 18 F-FDG sum image was created and used for subsequent analysis.…”

“…Activity of MAO-B increases in AD patients' brains; the enzyme is overexpressed in reactive astrocytes, and significant numbers of astrocytes surround both fibrillar and diffuse Ab plaques in postmortem AD brain tissue (18,19). A recent autoradiography study (20) suggested 11 C-DED as a suitable in vivo PET ligand for assessing MAO-B in AD brains.…”

Monoamine Oxidase Inhibitors—Revisiting a Therapeutic Principle

“…MAO-B is elevated in plaque-associated glia in Alzheimer brain. Upregulated MAO-B enzyme levels are mainly generated through neuroinflammatory response on the formation of AD plaques (Jossan, Ekblom, Aquilonius, & Oreland, 1994;Saura et al, 1994).…”

Monoamine oxidase inhibitors: Promising therapeutic agents for Alzheimer’s disease (Review)

“…Furthermore, oxidative stress and neuroinflammation are critical in the pathogenic cascade of neurodegeneration in AD, suggesting that therapeutic efforts aimed at these two mechanisms may be beneficial. It has been evidenced that several MAO inhibitors restrain the production of Aβ by inhibiting neuroinflammation, such as the inhibition of nuclear factor κB activity, the downregulation of the expression of interleukin 1β and tumor necrosis factor α, and the limitation of glial activation (38,128,129).…”