Monday morning's highlight was the Experience-Dependent Synaptic Plasticity and Neurogenesis in the Degenerating and Injured Brain nanosymposia session.
Carl Cotman, professor of neurology at UC Irvine and a potential mentor, spoke about the effects of exercise in mice, canines and humans. Dr. Cotman specializes in Alzheimer's (AD) research, and presented a collection of studies highlighting the effect of exercise on blood flow, amyloid aggregation and instance of BDNF. In transgenic mouse models of AD (Tg2576), Cotman discussed reduced amyloid and increased BDNF with exercise. In humans with AD, increased vessel volume and blood flow was observed with fast walking, corroborative with decreased amyloid reported by Liang et al in the Annals of Neurology this year.
Most notably, Dr. Cotman proposed that the brain "has a memory for exercise." Exemplifying this statement was his study from 2005 where AD rats exercised on a treadmill for one week, resulting in increased BDNF in the hippocampus. Some of these rats proceeded without exercise in the following week which resulted in decreased BDNF levels. These levels increased rapidly when the animals were exercised for an additional week to levels beyond those revealed due to the initial exposure, a phenomenon that typically takes weeks to induce in naive rats. This "memory for exercise" may prove to be key in designing rehabilitative exercise programs.
Mike Jakowec and Giselle Petzinger, respectively professor and clinician-researcher at USC, represented the recent work of their labs as well as the strong collaborative efforts within USC's Neuroscience labs. Advocate of exercise in rodent models of Parkinson's disease, Dr. Petzinger presented evidence that exercise may be working through the indirect dopamine pathway (D2) to aide motor recovery. Mot strikingly to me, their lab has reported that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) results in dopamine neuron spine loss specific to the D2 pathway via [F]Fallypride radiotracing (PET scan). Exercise in their MPTP mouse model results in a 98% increase in the striatal D2 receptor. This research suggests some very interesting targets for intervention.
The David Kopf lecture on Neuroethics was given this year by Hank Greely, professor of law at Stanford, and a professor by courtesy of genetics at the School of Medicine. Beyond delivering a lecture as eloquently as one will ever hear, the poignant stars of Dr. Greely's talk were copious.
Dr. Greely opened by saying that the "ethical issues of neuroscience are 10 years behind those in genetics," referring to the paradigm sweeps that genetic discoveries have prompted (i.e. eugenics). He elaborated that the implications of neuroscientific discovery were "more important than [those of] genetics, made so by immediacy and power." Namely, neurological dysfunction has very present consequences, whereas genetic abnormalities must emerge on the physiological level before they can be acted upon. For instance, if you were to find yourself predisposed to Alzheimer's through genetic testing, you would be protected from discrimination by the Genetic Information Non-discrimination Act of 2008. However, there exists no such protection if you are diagnosed via MRI.
Humans as mind-readers, MRI's distinguishing between conscious and unconscious vegetative states, and the responsibility of humanity to discern what is an adverse disease and what is just a condition that makes "us" (the indirectly affected "us") uncomfortable: these are some of many issues with which neuroscientists can become dangerously dissociated, but the bench does not separate us from the issues produced by our discoveries. The mindfulness of scientists guides social consequences.
I refer readers to Stanford's Neuroblog and The Neuro Dilettante for more adequate coverage of Greely's lecture.
Liang KY, Mintun MA, Fagan AM, Goate AM, Bugg JM, Holtzman DM, Morris JC, & Head D (2010). Exercise and Alzheimer's disease biomarkers in cognitively normal older adults. Annals of neurology, 68 (3), 311-8 PMID: 20818789
Adlard, P. (2005). Voluntary Exercise Decreases Amyloid Load in a Transgenic Model of Alzheimer's Disease Journal of Neuroscience, 25 (17), 4217-4221 DOI: 10.1523/JNEUROSCI.0496-05.2005
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