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<p class="publishdate"><span property="dc:date" datatype="xsd:dateTime" content="2018-09-25T00:00:00-04:00" class="date-display-single">September 25, 2018</span></p><div class='syndicate'><h1>Exercise and new nerve cell growth in Alzheimers disease</h1><div class="callout callout-with-border"><h3>At a Glance</h3>
<ul>
<li>In a mouse model of Alzheimers disease, exercise stimulated the growth of new nerve cells in the brain and reduced memory problems.</li>
<li>The researchers were able to design treatments to mimic some of the beneficial effects of exercise.</li>
<li>The findings pave the way for studies in people with Alzheimers disease.</li>
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<picture title="Illustration of neurons">
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-tiny/public/news-events/research-matters/2018/20180924-neurons.jpg?itok=UUWZvtFy&amp;timestamp=1537812093 1x" media="screen and (min-width: 0)" />
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<img src="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-medium/public/news-events/research-matters/2018/20180924-neurons.jpg?itok=g2p87cST&amp;timestamp=1537812093" alt="Illustration of neurons" title="Illustration of neurons" />
</picture><span class="caption">Researchers have been working to understand how Alzheimers disease disrupts the growth of new neurons in the brain.</span><span class="credit">maksime/iStock/Getty Images Plus</span></div>
</div><p>Experts estimate that more than 5 million Americans may have Alzheimers disease, the most common form of dementia. This irreversible brain disorder gradually worsens and destroys memory and thinking skills. Current treatments may slow memory loss, but theres no cure. There is some evidence that exercise can reduce the risk of cognitive decline during aging and decrease the risk of dementia, but studies with people have had mixed results.</p>
<p>Many changes take place during the course of Alzheimers disease, even before symptoms develop. Starting in the hippocampus region of the brain, abnormal deposits of proteins form amyloid plaques and tau tangles. Neurons (nerve cells) there stop functioning, lose their connections with other neurons, and die. Previous research with mice has suggested that theres also a disruption in neurogenesis, the process of new neurons arising from progenitor cells, in the hippocampus.</p>
<p>A research team led by Dr. Rudolph Tanzi of Massachusetts General Hospital and Harvard Medical School set out to investigate whether spurring growth of new hippocampus neurons could lessen memory problems in a mouse model of Alzheimers disease. The work was funded in part by NIHs National Institute on Aging (NIA) and National Institute of Mental Health (NIMH). Results were published in <em>Science </em>on September 7, 2018.</p>
<p>The researchers used mice engineered to develop an early, aggressive form of Alzheimers disease. The mice were injected with a compound known to boost survival of progenitor cells as well as a gene therapy that enhances proliferation of progenitor cells. The two treatments promoted the growth of nerve cells in the mice. However, the mice werent any better at a maze that tests memory.</p>
<p>The team also tested the effects of exercise. Untreated mice given access to an exercise wheel had new growth of nerve cells and performed better on memory tests. In addition, plaques and several proteins linked to Alzheimers disease, such as brain-derived neurotrophic factor (BDNF), improved in these mice.</p>
<p>Next, the research team tested the effects of combining the progenitor cell treatments with BDNF promotion. This combination, like exercise, promoted nerve cell growth and improved memory. It had these effects, however, without affecting plaques and other disease markers.</p>
<p>Blocking new growth of nerve cells in the hippocampus by various methods, in contrast, worsened memory and reduced BDNF. This finding suggests that the absence of new hippocampal neurons may play a role in Alzheimers disease.</p>
<p>“The lesson learned was that it is not enough just to turn on the birth of new nerve cells, you must simultaneously clean up the neighborhood in which they are being born to make sure the new cells survive and thrive,” Tanzi says. “Exercise can achieve that, but we found ways of mimicking those beneficial cognitive effects by the application of drugs and gene therapy that simultaneously turn on neurogenesis and BDNF production.”</p>
<p>More research is needed to determine whether these findings extend beyond this mouse model of Alzheimers disease. If they prove relevant to human disease, they may lead to new ways to prevent or treat dementia.</p>
<p>—by Geri Piazza</p></div><h2 class="label-above">Related Links</h2><ul class="spaced print-urls"><li><a href="https://www.nih.gov/news-events/nih-research-matters/compound-repairs-features-alzheimers-disease-mice" target="_top">Compound Repairs Features of Alzheimers Disease in Mice</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/drug-improves-alzheimers-condition-mice" target="_top">Drug Improves Alzheimers-like Condition in Mice</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/clues-alzheimers-disease" target="_top">Clues to Alzheimers Disease</a></li><li><a href="https://www.nih.gov/news-events/nih-research-matters/mediterranean-diet-may-slow-development-alzheimers-disease" target="_top">Mediterranean Diet May Slow Development of Alzheimers disease</a></li><li><a href="https://newsinhealth.nih.gov/special-issues/seniors/dealing-dementia" target="_top">Dealing with Dementia</a></li><li><a href="https://www.nia.nih.gov/health/alzheimers" target="_top">Alzheimer's Disease &amp; Related Dementias</a></li></ul><p class="footnote"><strong class="label-inline">References:&nbsp;</strong><a href="https://www.ncbi.nlm.nih.gov/pubmed/30190379">Combined adult neurogenesis and BDNF mimic exercise effects on cognition in an Alzheimer's mouse model</a>. Choi SH, Bylykbashi E, Chatila ZK, Lee SW, Pulli B, Clemenson GD, Kim E, Rompala A, Oram MK, Asselin C, Aronson J, Zhang C, Miller SJ, Lesinski A, Chen JW, Kim DY, van Praag H, Spiegelman BM, Gage FH, Tanzi RE. <em>Science</em>. 2018 Sep 7;361(6406). pii: eaan8821. doi: 10.1126/science.aan8821. PMID: 30190379.</p><p class="footnote"><strong class="label-inline">Funding:&nbsp;</strong>NIHs National Institute on Aging (NIA) and National Institute of Mental Health (NIMH); Cure Alzheimers Fund; JPB Foundation; Henry and Allison McCance Center for Brain Health at Massachusetts General Hospital; Mathers Foundation; and Leona M. and Harry B. Helmsley Charitable Trust.</p>
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