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P3‐078: Mild cognitive impairment: Classification methods and two‐year dementia conversion rates
Author(s) -
Cholerton Brenna,
Baker Laura,
Trittschuh Emily,
Larson Eric,
Crane Paul,
McCurry Susan,
McCormick Wayne,
Bowen James,
Saucedo Hector Hernandez,
Arbuckle Matthew,
Craft Suzanne
Publication year - 2012
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2012.05.1297
Subject(s) - dementia , neuropsychology , cognition , psychology , normative , cohort , neuropathology , cognitive test , clinical psychology , medicine , audiology , psychiatry , disease , philosophy , epistemology
disorder characterized by amajor degeneration of the brain cortex with presence of extracellular amyloid plaques, intra-neuronal fibrillary tangles and neuronal cell loss in specific cortical and subcortical areas. Ab is the major component of amyloid plaques and is considered to play a crucial role in the progression of AD. Several lines of evidence suggest that these Ab peptides induce neuronal apoptosis, resulting in neurodegeneration and cognitive dysfunction. N-trans feruloyltyramine (NTF), purified from a traditional medicine tree, Polyalthia suberosa, has been suggested to be a potent anti-oxidant. In the present study, we examined the protective effect of NTF against Ab 1-42 -induced cytotoxicity, Bax, caspase 3 and reactive oxygen species (ROS) in cultured rat cortical neurons.Methods: Primary cultured neurons were treated with 0, 25, 50 and 100 mMNTF for 1 hour before the addition of 10 mM oligomeric Ab1-42 at sublethal dose, followed by incubation for a further 24 hour prior to cell viability (MTTassay) determination, Western blotting and ROS formation assay. Conclusions: Exposure of cultured cortical neurons to 10 mM A b 1-42 for 24 hours caused apoptotic cell death, as evidence by morphological changes and presence of activated caspase-3 and pro-apoptotic Bax protein, which could be attenuated by pretreatment with NTF (25-250 mM for 1 hour). Apoptotic cell death was accompanied by elevated levels of ROS. These findings suggest that the protective effect of NTF against Ab1-42-induced neuronal death might be due to its antioxidative property.