Action is unsatisfactory for two reasons: 1) in accordance with the observations reported by Hudson et al. resveratrol biases the Thioflavin T fluorescence assay for amyloid fibril detection through nonspectral interferences.2) In the context of AD, anti-aggregative drugs might exert more harm than as amyloid oligomers are more toxic than fibrils. We performed our CR assay to detect the presence of amyloid fibrils in the presence of resveratrol and found, that the compound does not influence Ab-metal complexes aggregative pathway, except for Ab-Cu where we observed an increase in fibrillization. One possible explanation could be that resveratrol stabilizes Ab-Cu complex in more ordered structures because of its Cu chelating properties. In agreement with the CR assay, TEM micrographs do not show an anti-amyloidogenic effect of resveratrol. Brain-derived neurotrophic factor has multiple neuroregulatory functions and one of its major targets are GABAergic neurons, which play essential role in oscillatory activity of neuronal networks. Among several types of brain oscillations, gamma oscillations, which include frequencies ranging from 25 to 100 Hz, draw a lot of attention, because they are considered an integrating mechanism, which couples different brain structures during memory encoding and retrieval. In addition, changes in gamma oscillatory activity in human brain have been found in several psychiatric illnesses including schizophrenia and bipolar disorder. Hippocampus is one of the brain areas generating gamma oscillations, which are Nifedipine driven by a network of connected inhibitory neurons and require GABAergic transmission. Fast-spiking Oxybutynin chloride parvalbumin-positive interneurons in particular are thought to be responsible for driving gamma oscillations and genetic attenuation of excitatory inputs in these neurons have been shown to reduce oscillation power in the hippocampal area CA3. Hippocampus, where oscillations are thought to be involved in cognition and memory, expresses high levels of BDNF, which has been proposed to modulate oscillations by influencing the firing of GABAergic neurons. Nevetherless, experimental evidence that BDNF modulates gamma oscillations via inhibitory neurons is lacking. In the hippocampus, BDNF is highly expressed in CA3 pyramidal neurons, which appear to deliver BDNF protein to area CA1 via the Schaffer collateral axons. Given that BDNF influences firing of GABAergic neurons, which are required for gamma oscillations in CA3 and CA1, we hypothesized that BDNF may modulate these oscillations. To test this hypothesis, we examined carbachol-induced gamma oscillations in hippocampal slices from conditional BDNF knockout mice lacking BDNF gene in the CA3 pyramidal neurons. In these slices, the oscillation power was reduced in CA1, but not CA3, when compared to slices from wild type mice; yet, this reduction was partially reversed in the presence of tropisetron, an inhibitor of 5HT3 receptor, whose expression was elevated in KO mice.