Ben Barres on Channel-mediated tonic GABA release from glia.

COMMENT These are controversial findings and need corroboration. It would be interesting to confirm that the Bestrophin 1 (Best1) anion channel purported to release GABA from glia is expressed in these cells. The authors did not carry out in situ hybridization to

PAPER Lee S, Yoon BE, Berglund K, Oh SJ, Park H, Shin HS, Augustine GJ, Lee CJ

Channel-mediated tonic GABA release from glia.

Science. 2010 Nov 5;330(6005):790-6. PubMed: 20929730

Kelly Dineley on Mossy fiber long-term potentiation deficits in BACE1 knock-outs can be rescued by activation of alpha7 nicotinic acetylcholine receptors.

COMMENT In this manuscript, Wang et al. detail an investigation into a presynaptic form of NMDA-independent LTP (mfLTP) at the mossy fiber—CA3 synapse in mice lacking β-secretase (BACE1)—BACE KO. They report that the mfLTP deficits can be rescued by activation of

PAPER Wang H, Song L, Lee A, Laird F, Wong PC, Lee HK

Mossy fiber long-term potentiation deficits in BACE1 knock-outs can be rescued by activation of alpha7 nicotinic acetylcholine receptors.

J Neurosci. 2010 Oct 13;30(41):13808-13. PubMed: 20943921

Gerard Drewes on Epothilone D improves microtubule density, axonal integrity, and cognition in a transgenic mouse model of tauopathy.

COMMENT The authors demonstrate clear beneficial effects of low concentrations of epothilone D, a brain-permeable microtubule-stabilizing agent, on transgenic mice that develop forebrain tau inclusions. Similar approaches using the marketed cancer drug paclitaxel

PAPER Brunden KR, Zhang B, Carroll J, Yao Y, Potuzak JS, Hogan AM, Iba M, James MJ, Xie SX, Ballatore C, Smith AB, Lee VM, Trojanowski JQ

Epothilone D improves microtubule density, axonal integrity, and cognition in a transgenic mouse model of tauopathy.

J Neurosci. 2010 Oct 13;30(41):13861-6. PubMed: 20943926

Murat Durakoglugil on Apolipoprotein E4 causes age- and Tau-dependent impairment of GABAergic interneurons, leading to learning and memory deficits in mice.

COMMENT Yadong Huang and colleagues have previously shown that ApoE plays an important role in adult hippocampal neurogenesis, and the ApoE4 isoform impairs GABAergic input to newborn neurons (1). In this follow-up paper, they describe the functional significance

Joachim Herz on Apolipoprotein E4 causes age- and Tau-dependent impairment of GABAergic interneurons, leading to learning and memory deficits in mice.

COMMENT This paper by Huang and colleagues points toward an interesting role of GABAergic interneurons as potential intermediaries in the pathogenesis of Alzheimer disease. Although the mechanisms by which ApoE4 predisposes to AD are still under lively debate, th

PAPER Andrews-Zwilling Y, Bien-Ly N, Xu Q, Li G, Bernardo A, Yoon SY, Zwilling D, Yan TX, Chen L, Huang Y

Apolipoprotein E4 causes age- and Tau-dependent impairment of GABAergic interneurons, leading to learning and memory deficits in mice.

J Neurosci. 2010 Oct 13;30(41):13707-17. PubMed: 20943911

Michela Deleidi

United States

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