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Journal of Neuroscience
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src="https://www.jneurosci.org/sites/default/files/styles/large/public/highwire/jneuro/44/48.cover-source.jpg?itok=CjIRIFvd" alt="The Journal of Neuroscience: 44 (48)" /></a></div></div> </div> </div> </div> </div> <div class="panel-panel panel-col-last"> <div class="inside"><div class="panel-pane pane-highwire-markup" > <h2 class="pane-title">About the Cover</h2> <div class="pane-content"> <div class="highwire-markup"><div xmlns="http://www.w3.org/1999/xhtml" id="content-block" xmlns:xhtml="http://www.w3.org/1999/xhtml"><div><span class="highwire-journal-article-marker-start"></span><div class="caption cover-img"><p id="p-1">Shown is a cortical neuron with CD2AP tagged with green fluorescent protein to show its expression. Fluorescence was color-coded from blue (at its brightest) to yellow (dimmer) to highlight where CD2AP is expressed in dendritic spines. Loss of function variants of the CD2AP gene may contribute to late-onset Alzheimer's disease. The technique used in this image helped uncover whether loss of CD2AP function contributes to synaptic dysfunction, which is one of the causal mechanisms for late-onset Alzheimer's disease. See <a href="https://doi.org/10.1523/JNEUROSCI.1734-23.2024">Farzaneh S. Mirfakhar et al.</a> for more information on how a variant of this gene contributes to synapse dysfunction. 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