Normal aging, motor neurone disease, and Alzheimer's disease are characterized by cortical changes in inflammatory cytokines.

The role of increased brain inflammation in the development of neurodegenerative diseases is unclear. Here, we have compared cytokine changes in normal aging, motor neurone disease (MND), and Alzheimer's disease (AD). After an initial analysis, six candidate cytokines, interleukin (IL)- 4, 5, 6, 10, macrophage inhibitory protein (MIP)-1α, and fibroblast growth factor (FGF)-2, showing greatest changes were assayed in postmortem frozen human superior frontal gyri (n = 12) of AD patients, aging and young adult controls along with the precentral gyrus (n = 12) of MND patients. Healthy aging was associated with decreased anti-inflammatory IL-10 and FGF-2 levels. AD prefrontal cortex was associated with increased levels of IL-4, IL-5, and FGF-2, with the largest increase seen for FGF-2. Notwithstanding differences in the specific frontal lobe gyrus sampled, MND patients' primary motor cortex (precentral gyrus) was associated with increased levels of IL-5, IL-6, IL-10, and FGF-2 compared to the aging prefrontal cortex (superior frontal gyrus). Immunocytochemistry showed that FGF-2 is expressed in neurons, astrocytes, and microglia in normal aging prefrontal cortex, AD prefrontal cortex, and MND motor cortex. We report that healthy aging and age-related neurodegenerative diseases have different cortical inflammatory signatures that are characterized by increased levels of anti-inflammatory cytokines and call into question the view that increased inflammation underlies the development of age-related neurodegenerative diseases.

Açaí (Euterpe oleraceae Mart.) berry extract exerts neuroprotective effects against ß-amyloid exposure in vitro.

The native South American palm açaí berry (Euterpe oleraceae Mart.) has high polyphenolic and antioxidant levels. This study examined whether açaí berry extract afforded protection against ß-amyloid (Aß)-mediated loss of cell viability and oxidative stress associated with anti-fibrillar effects. PC12 cells were exposed to either Aß1-42, Aß25-35 or tert butyl hydroperoxide (t-BHP), alone or in the presence of açaí extract (0.5-50µg/ml). Thioflavin T (ThT) binding assay and transmission electron microscopy were used to determine effects of açaí extract on Aß1-42 fibril morphology and compared to açaí phenolics gallic acid, cyanidin rutinoside and cyanidin glucoside. Exposure to Aß1-42, Aß25-35 or t-BHP decreased PC12 cell viability. Pretreatment with açaí extract significantly improved cell viability following Aß1-42 exposure, however Aß25-35 or t-BHP-mediated viability loss was unaltered. Açaí extract inhibited ThT fluorescence and disrupted Aß1-42 fibril and aggregate morphology. In comparison with other phenolics, açaí was most effective at inhibiting Aß1-42 aggregation. Inhibition of ß-amyloid aggregation may underlie a neuroprotective effect of açaí.