Scenes from NYU’s Brain Fair as part of BraiNY on March 13, 2013.
- 25th March
2013 - 25
- 13th March
2013 - 13
Inside the NYU Community Brain Fair
Hi guys!
Just wanted to give you an update regarding the NYU Community Brain Fair and NYC Brain Awareness Week… In regards to the Brain Fair, we’re still here! So feel free to drop by and visit one of our many exhibits. Topics covered include : History of Neuroscience, Top 10 Brain Myths, Famous Brains (think H.M., Oliver Sacks, and Chuck Close), Chemical Senses, Alzheimer’s Disease, Parkinson’s Disease, Addiction Pathways, Caloric Sensing in Flies, Neuroeconomics and Neuropsychology. The Neuroanatomy table even has real human brains on display for the oddly curious :)
Other hands-on exhibits include risk discounting games, optical illusions the jelly bean flavor experiment, observing C. elegans mutants under the microscope, and playing a reward related game that resembles beer pong!
Also, we tried to have something for everyone and we even have a Kids table with (anatomically correct) brain hats, arts and crafts, brain mazes, etc…
If you can’t make it, that’s ok! Click here for other braiNY events you can make it to.
Pictures coming later!
- 1st November
2012 - 01
Sandy wipes out NYU lab mice, a huge setback for medical research
If researchers sent some mice genes to other universities, they can get copies. If not, they start from scratch.
As a member of the NYU neuroscience community, my heart goes out to all those researchers that lost animals during hurricane Sandy. Luckily, our lab’s animal facility is not located at the NYU Langone Medical Center so I didn’t lose any animals. Others, as discussed in the article, were not so lucky. I can’t help but wonder what the repercussions of this will be for all those graduate students/postdocs trying to move their thesis defenses and career plans forward. Valuable lessons were learned, but the cost may have been too high…
- 13th October
2012 - 13
Meet My Class: Due to the wide variety of topics in neuroscience and my specific interests, I have decided to introduce you to some of my fellow classmates at the NYU Sackler Institute. These people are all very bright and amazingly talented individuals who are very passionate about their work and are willing to share it with a broader audience- you!
First up in the Meet My Class series- Dave Marzan. Dave Marzan received his B.S. from University of California- San Diego (UCSD, one of the top neuroscience institutions in the country). Dave and I met during NYU interviews a little over 3 years ago and have been friends ever since. He has an amazing attitude and his excitement regarding neuroscience is contagious. He is also part of the Society for Neuroscience Scholars Program (NSP). Needless to say, I feel very lucky to have him as a fellow classmate and he has happily accepted my invitation to write about his work. The image above was captured by him recently and was presented today at the NSP Diversity Poster session at SfN NOLA.
Here it goes, in Dave’s own words…
Contrary to popular belief, the brain is not comprised of only neurons. 90% of central nervous system cells (CNS) are glia. One type of glia in the CNS, oligodendrocytes, form the wrapping around axons and support proper neuron function. Multiple sclerosis (MS) is the most common cause of inflammatory neurological disability in young adults. Inflammation and autoimmune reactivity against the myelinating cells of the nervous system causes demyelination, axonal damage andneurodegeneration. The CNS is capable of spontaneous remyelination by stem cells and oligodendrocyte precursor cells (OPCs). However,remyelination significantly decreases with age; this failure of remyelination is thought to be a major contributor to MS progression.While there has been progress in slowing autoimmune mediated demyelination, there has been none in promoting regeneration and reversing disease progression. Research in regenerative therapies has the potential to benefit the 400,000 MS patients in America as well as countless others suffering from neurodegenerative diseases.
As a graduate student at NYU, I work in the lab of James Salzer,
a leading expert in the genetic and cellular mechanisms governing
myelination. My project focuses on studying how the brain’s immune
cells , microglia, contribute to the process of demyelination and
remyelination in vivo. To this end, I employ a novel trangenic mouse
line that allows for inducible deletion of microglia from the CNS. I
remove microglia at time points critical for developmental myelination, toxin induced demyelination and endogenous remyelination in order to study their function. Understanding how these immune cells contribute to degeneration and regeneration can provide insight into the pathophysiology of MS and in the development of regenerative therapies.
The image above is a immunofluorescent confocal projection taken from an adult mouse. The green cells are PDGFRα+ oligodendrocyte precursor cells (OPCs) migrating into the corpus callosum to differentiate into oligodendrocytes and form new myelin (red). Green OPCs are enriched in the corpus callosum because the mouse was placed on a demyelinating diet and these cells are migrating to site of injury to remyelinate. Blue is a nuclear hoechst stain that stains all cell types.
To visit the Salzer Lab page, click here.
- 9th June
2010 - 09
I took these pictures last semester.
We were being taught how to do immunocytochemistry, a laboratory technique in which a specific antibody is used to detect the presence of a particular antigen or protein in a cell. Because the antibody is specific for the protein of interest, it binds the protein and allows visualization by staining and examination under a microscope. Naturally, darker staining relates to protein concentration in those particular areas.
We were given an antibody and were told to determine what protein it was specific for by staining and visualizing our samples. After a long search, I came up with Calbindin D, a calcium-binding vitamin D dependent protein which helps transport calcium. It’s localization includes the cerebellum & cerebellar cortex, the hippocampus and the dentate gyrus, as well as the striatum and other components of the basal ganglia.
- 15th May
2010 - 15
Olfactory Dysfunction as an Early Marker of Alzheimer’s
A study conducted by research groups at the Nathan Kline Institute for Psychiatric Research in upstate New York has found a link between loss of smell function in Alzheimer’s disease (AD) with amyloid plaque accumulation in the brain, one of the hallmarks in AD. Their work suggests that olfactory dysfunction, usually a common symptom in AD patients, may serve as an early diagnostic tool for the disease.
Their findings include:
The real value in this research, I believe, is that many behavioral symptoms associated with AD occur or have their onset early in life. Loss of smell has been pinpointed as one of them, and this study suggests that it may be more helpful as a diagnostic tool than brain degeneration (which usually occurs as the disease gets progressively worse). Thus, loss of smell is a inexpensive diagnostic tool that may help in earlier therapeutic interventions.
Wesson, DW, Levy, E, Nixon, RA, Wilson, DA. 2010. Olfactory dysfunction correlates with amyloid-beta burden in Alzheimer’s disease mouse model. Journal of Neuroscience. 30 (2): 505-514.
