Neuroimage. 2007 May 1;35(4):1401-8.
Some in vitro models of alzehimers disease (AD) show a decreased rate of axonal transport linked with accumulations of tau and amyloid-B (AB) proteins. Adding AB to cultured neurons also inhibits transport, possibly through interactions with actin that change its level of polymerization. The aim of this study was to develop a new way to measure in vivo axonal transport. To study in vivo transport rates, the group used MEMRI and a strain of mouse which expressed an aggressive mutant form of amyloid precursor protein and accumulations of AB plaques. Mice were given Mn through nasal lavage and repeatedly imaged for an hour to see how transport to and uptake into the olfactory bulbs occurred. Post-Mn signal intensities were normalized to pre-Mn levels to find when Mn had reached regions of interest. As expected, MRI signals incrased over time in manganese-treated mice, but it did not increase in control animals. They then used decreased temperature and cholchicine (which prevents polymerization of actin microtubules) to show that by inhibiting axonal transport, they could prevent the the transport-dependent increase in signal intensity observed in control animals.
To look at developing an assay for diagonsing AD, they used MEMRI and a model of mouse which expressed a mutant form of amyloid precursor protein and increasing accumulations of AB plaques with age. They found that after manganese treatment, young AD mice showed similar transport rates (as demonstrated by MEMRI signal increases) to regular mice, but the signal was reduced in 7-8 month old mice, and reduced even further in 11-14 month old mice. This is cool because there aren't currently good ways to diagnoze alzheimers disease while a person is still alive. Diagnosis is usually done post-mortem, after years of AD-like symptoms. Finding a way to diagnose it in the early stages might be a great way to prevent it from getting worse before it's too late to treat. -DH
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