A copy of this work was available on the public web and has been preserved in the Wayback Machine. The capture dates from 2011; you can also visit <a rel="external noopener" href="http://www.nmr.mgh.harvard.edu/~bradd/library/seeley_neuron_2009.pdf">the original URL</a>. The file type is <code>application/pdf</code>.
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<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/skzqffpatvawfgf7uspguqs4yu" style="color: black;">Alzheimer's & Dementia</a>
During development, the healthy human brain constructs a host of large-scale, distributed, function-critical neural networks. Neurodegenerative diseases have been thought to target these systems, but this hypothesis has not been systematically tested in living humans. We used network-sensitive neuroimaging methods to show that five different neurodegenerative syndromes cause circumscribed atrophy within five distinct, healthy, human intrinsic functional connectivity networks. We further<span class="external-identifiers"> <a target="_blank" rel="external noopener noreferrer" href="https://doi.org/10.1016/j.jalz.2010.05.522">doi:10.1016/j.jalz.2010.05.522</a> <a target="_blank" rel="external noopener" href="https://fatcat.wiki/release/dd3jz4n2kfdidnqheao2lbfhu4">fatcat:dd3jz4n2kfdidnqheao2lbfhu4</a> </span>
more »... ed a direct link between intrinsic connectivity and gray matter structure. Across healthy individuals, nodes within each functional network exhibited tightly correlated gray matter volumes. The findings suggest that human neural networks can be defined by synchronous baseline activity, a unified corticotrophic fate, and selective vulnerability to neurodegenerative illness. Future studies may clarify how these complex systems are assembled during development and undermined by disease. 42 Neuron 62, 42-52, April 16,
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