PAPER Shirahama-Noda K, Yamamoto A, Sugihara K, Hashimoto N, Asano M, Nishimura M, Hara-Nishimura I
John Cirrito on Regulation of Presynaptic Ca2+, Synaptic Plasticity and Contextual Fear Conditioning by a N-terminal β-Amyloid Fragment.
COMMENT This study by Lawrence et al. on the activity of the N-terminal fragment of Aβ raises some important questions regarding the physiological roles of APP cleavage products. As APP is cleaved, it makes sense that the products could serve as activity ...
Erik Portelius on Regulation of Presynaptic Ca2+, Synaptic Plasticity and Contextual Fear Conditioning by a N-terminal β-Amyloid Fragment.
COMMENT From when we first discovered that the β/α generated fragment Aβ1-15 increased in response to γ-secretase inhibitor (GSI) treatment, we have wondered whether inducing the α-secretase pathway is “good or bad.” Lawrence and colleges clearly show that ...
Stanford University School of MedicineStanford, United States
Laboratory of Medical Physics, Medical School, Aristotle University of ThessalonikiThessaloniki
Pune , India
ANTIBODY monoclonal 1D3 manufacturer Ovalbumin-conjugated linear peptide corresponding to human TDP-43 phosphorylated at serine 409 and 410. Purified in buffer containing 0.1 M Tris glycine with 0.05% sodium azide This antibody recognizes human TDP-43 ...
RESEARCH NEWS 2014-10-29 Research News In large quantities, Aβ poisons synapses; in small amounts, it can enhance plasticity. What explains this dual action? In the October 22 Journal of Neuroscience, researchers led by Robert Nichols at the University of Hawaii at Manoa, ...
No filters selected