Professor Stephen Grossberg, BU’s Wang Professor of Cognitive and Neural Systems and a professor of mathematics, psychology, and biomedical engineering, has received the 2017 IEEE Frank Rosenblatt Award from the Institute of Electrical and Electronics Engineers (IEEE). Grossberg won the prize for his work in cognition and brain behavior, and for demonstrating how technology can emulate neural processes. His research has encompassed memory, learning, human speech and motor control, and vision, among other topics.
Come to the hooding ceremony to congratulate your fellow students! Thursday May 12th 2:00 PM Agganis Arena. Stay tuned for information about our first GPN Graduation Reception.
Congratulations to our new PhDs!!
Caitlin (Monaghan), Chelsea (Trengrove), Emily (Stephen), Franne (Kamhi), Jason (Climer), Lissa (Riley), Marie-Pierre (Payen), Nick (James), and Nick (Robinson).
Congratulations to Mariel Seiglie and Cassie Moore (GPN students in the Addiction Specialization) win the ASPET (American Society for Pharmacology and Experimental Therapeutics) student travel awards to the annual meeting this April in San Diego.
A special congratulations from our community to Dr. Marc Howard for his promotion to Full Professor in the Department of Psychological & Brain Sciences!
Congratulations to you all and remember we are always your family when you need us. You made it!
A huge congratulations to our colleague Stephen Grossberg for the coveted award from the Society of Experimental Psychologists.
The Society of Experimental Psychologists gave its 2015 Norman Anderson Lifetime Achievement Award to Stephen Grossberg, Wang professor of cognitive and neural systems and professor of mathematics and psychology, for his pioneering theoretical research on how brains give rise to minds.
The Society (SEP) is an academic society for experimental psychologists that meets annually to conduct plenary sessions with its members. Their objective is to “advance psychology by arranging informal conferences on experimental psychology.” With only 5-10% of experimental psychologists holding membership, admittance to the SEP is a great honor.
Another great acknowledgment of outstanding accomplishment for our dear colleague Nancy Kopell comes from Israel Brain Technologies. Nancy is a member of the National Academy of Sciences and the American Academy of Arts and Sciences. She is an honorary member of the London Mathematical Society, a distinction given to only one or two mathematicians each year. She is a recipient of a MacArthur genius award and Sloan and Guggenheim fellowships.
Boston University Neuroscience students volunteer at Massachusetts State Science and Engineering Fair
Boston University Neuroscience graduate students volunteered at the 2015 Massachusetts State Science and Engineering Fair! BU graduate students include: Andres Salazar Gomez, Emily Stephen, Frannie Kamhi, Adam Vogel, Kayle Sawyer. Also pictured is Emily Kate McDonough from the University of Massachusetts.
Congratulations to Professor Tsuneya Ikezu and Colleagues for Selection in the Neuroscience 2014 Press Conference
Tau’s Role in Neurodegeneration
Microglia and exosome-mediated spread of pathogenic tau in Alzheimer’s disease
Our study suggests that microglial uptake and spreading of tau protein may play an important role in Alzheimer’s disease. Alzheimer’s disease is a neurodegenerative disease that affects more than 5.3 million people in the United States. The average life expectancy is eight to 10 years after onset, and there is currently no preventive or curative drug for this devastating disease. Alzheimer’s disease is characterized by the two different globs of proteins: beta-amyloid plaques and neurofibrillary tangles.
This study focuses on neurofibrillary tangles, which comprise aggregates of a protein called tau, normally attached to the cytoskeleton to build and maintain nerve cell structure. Tau accumulation first appears in the specific human brain region called the transentorhinal cortex before the onset of symptoms, and then gradually spreads to the hippocampal region. Because the hippocampus is important for learning and memory, the spread of tau protein in this region is associated with the early signs of Alzheimer’s disease. The mechanism by which tau protein spreads in specific brains is one of the hottest topics in the Alzheimer’s disease research field. Halting this spread before the onset of disease symptoms is a promising preventive intervention for the disease.
We hypothesize that brain immune cells called microglia engulf tau-containing synapses, or nerve cell bodies, and secrete tiny particles containing the tau protein. These particles are called exosomes, which are small vesicles of 50-100 nm in diameter and contain many messenger molecules and brain disease-linked proteins such as prion protein and alpha-synuclein. Exosomes can spread tau protein to other nerve cells and may serve as seeding molecules for inducing the aggregation of tau protein in the recipient cells. This microglial uptake and spreading of tau may play an important role in neurofibrillary tangle development.
Overall, our study demonstrates that exosomes and microglia are important mediators for spreading the pathogenic tau protein in tissue culture and animal models. Therefore, this study is highly significant not only to Alzheimer’s disease, but also to Pick’s disease and traumatic brain injury, in which neurofibrillary tangles also develop in the brain. In addition, this mechanism can be applied in understanding the spreading of other pathogenic molecules known to exist in the exosomes, such as prion protein for prion disease and alpha-synuclein for Parkinson’s disease.
*T. IKEZU1, H. ASAI2, S. IKEZU2, T. HAYDAR3, B. WOLOZIN1, S. KÜGLER4; 1Pharmacol. and Neurol., 2Pharmacol. and Exptl. Therapeut., 3Anat. and Neurobio., Boston Univ. Sch. of Med., Boston, MA; 4Ctr. for Nanoscale Microscopy and Physiol. of the Brain, Univ. Med. Göttingen, Göttingen, Germany
Presentation #: 578.08; Speaking Time: 11/18/2014 1:00:00 PM – 11/18/2014 3:00:00 PM
The neurofibrillary tangle is a pathological hallmark of Alzheimer’s disease (AD) and primarily consists of hyper-phosphorylated tau protein (pTau). pTau first appears in the entorhinal cortex in the presymptomatic stage, then gradually disseminates to the hippocampal region around the onset of clinical symptoms of AD. Halting this tau spread in the asympomatic stage is a promising therapeutic approach for AD. The exosome is a small vesicle of 50-100 nm in diameter, enriched in ceramide, and is suggested to contain neuropathogenic proteins, such as prion, α-synuclein, and recently tau proteins. A growing body of evidence suggests that microglia contribute to tauopathy-related pathogenesis in both human and animal models. We hypothesize that microglia transduce tau aggregates into nearby neuronal cells via exosomal secretion, and that inhibition of the exosome synthesis or secretory pathway reduces tau dissemination. We found that microglia efficiently phagocytose and secrete human tau aggregates in exosomes, which efficiently transduce tau aggregates in primary cultured mouse cortical neurons and induces accumulation of pTau. Moreover, we have created a novel mouse model exhibiting acute tau-spread by stereotaxic injection of adeno-associated virus expressing neuron-specific human mutant tau into the medial entorhinal cortex of mouse brain, which show spread of human tau to the granular cell layer of dentate gyrus at 28 days post injection. This tau spread was significantly suppressed by depletion of microglia or inhibition of neutral sphingomyelinase-2, which synthesizes ceramide and regulates exosome synthesis. These results demonstrate that microglia and exosomes play significant roles in spreading pathogenic tau in mouse brain. Our findings could lead to an entirely novel paradigm for delaying the progression of disease not only in AD but also other tauopathies such as FTD and chronic traumatic encephalopathy.