The aim of this study is to compare the elemental composition among different coffee varieties consumed in Jordan. Levels of different metallic elements in coffee samples; green and roasted coffee beans from five origins; Brazil, Ethiopia, Kenya, Columbia, and India, collected from the Jordanian market were investigated. Twenty-two elements, including essential and toxic elements such as potassium (K), magnesium (Mg), calcium (Ca), iron (Fe), aluminum (Al), manganese (Mn), copper (Cu), barium (Ba), strontium (Sr), zinc (Zn), chromium (Cr), lead (Pb), nickel (Ni), vanadium (V), cobalt (Co), gallium (Ga), uranium (U), cadmium (Cd), silver (Ag), lithium (Li), indium (In), bismuth (Bi), thorium (Th), and thallium (Ti), were determined using inductively coupled plasma-mass spectrometry (ICP-MS). The detected heavy metals and their intake per 1 cup of coffee did not largely contribute to the recommended daily intake (RDI) and tolerable upper limit of daily intake (TULD) in an adult with an average body weight of 80 kg. The ICP-MS versus flame atomic absorption spectrometry (FAAS) results were linearly fitted, and the correlation coefficients ( R2 > 0.95) were better than 0.95 for the three checked elements. No significant difference between the results of the two techniques was observed ( p > 0.05). The ANOVA results indicated the presence of a significant difference between the levels of Cr, Co, and Zn in green and roasted coffee beans. The results of this study indicated that the coffee consumed in Jordan did not contain toxic levels of heavy elements and is safe for consumption according to health organizations.

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Brain-derived neurotrophic factor (BDNF) dysregulations contribute to the neurotoxicity in neurodegenerative pathologies and could be efficiently targeted by therapies. In Alzheimer's disease (AD), although the relationship between BDNF and amyloid load has been extensively studied, how Tau pathology affects BDNF signaling remains unclear. Using the TAU-P301L transgenic zebrafish line, we investigated how early Tau-induced neurotoxicity modifies BDNF signaling. Alterations in BDNF expression levels were observed as early as 48 h post fertilization in TAU-P301L zebrafish embryos while TrkB expression was not modified. Decreasing BDNF expression, using a knockdown strategy in wild-type embryos to mimic Tau-associated decrease, did not modify receptor expression but promoted neurotoxicity as seen by axonal outgrowth shortening and neuronal cell death. Moreover, the TrkB antagonist ANA-12 reduced the length of axonal projections. Rescue experiments with exogenous BDNF partially corrected neuronal alterations in TAU-P301L by counteracting primary axonal growth impairment but without effect on apoptosis. Importantly, the axonal rescue was proved functionally effective in a behavioral test, at a similar level as obtained with the GSK3b inhibitor LiCl, used as positive control. Finally, treatment with a TrkB agonist, 7,8-dihydroxyflavone, gave comparable results and allowed full rescue of locomotor response. We provided here strong evidences that Tau neurotoxicity provoked alterations in BDNF system and that BDNF pathway might represent an efficient therapeutic target.