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The brain is an exceptionally complex organ that we have yet to fully understand. It has more than 80 billion neurons, making over 100 trillion connections to each other, which are responsible for behavior, memory, cognition, and more.

Developing a complete understanding of the brain and its functions requires expertise across many disciplines, from the biological sciences and chemistry to psychology and engineering. Recent advances in biotechnology and data science now allow researchers from different fields to bridge their separate approaches and work toward a comprehensive understanding of the brain.

Yale is taking full advantage of this new capability, integrating its renowned intellectual, academic, clinical, and technical resources into a neuroscience initiative. The result will be a multifaceted and revolutionary understanding of how the brain forms and works—and what underlies neurological disease, age-related neurodegeneration, and behavioral disorders. As the next decade gives rise to a paradigm shift in neuroscience with tremendous benefits to human health and welfare, Yale is determined to lead the way.

How Depression Affects The Brain - Yale Medicine Explains

For many people, depression turns out to be one of the most disabling illnesses that we have in society. Despite the treatments that we have available, many people are not responding that well. It's a disorder that can be very disabling in society. It's also a disorder that has medical consequences. By understand the neurobiology of depression we hope to be able more to find the right treatment for the patient suffering from this disease. The current standard of care for the treatment of depression is based on what we call the monoamine deficiency hypothesis. Essentially, presuming that one of three neurotransmitters in the brain is deficient or underactive. But the reality is, there are more than 100 neurotransmitters in the brain. And billions of connections between neurons. So we know that that's a limited hypothesis. Neurotransmitters can be thought of as the chemical messengers within the brain, it's what helps one cell in the brain communicate with another, to pass that message along from one brain region to another. For decades, we thought that the primary pathology, the primary cause of depression was some abnormality in these neurotransmitters, specifically serotonin or norepinephrine. However, norepinephrine and serotonin did not seem to be able to account for this cause, or to cause the symptoms of depression in people who had major depression. Instead, the chemical messengers between the nerve cells in the higher centers of the brain, which include glutamate and GABA, were possibilities as alternative causes for the symptoms of depression. When you're exposed to severe and chronic stress like people experience when they have depression, you lose some of the connections between the nerve cells. The communication in these circuits becomes inefficient and noisy, we think that the loss of these synaptic connections contributes to the biology of depression. There are clear differences between a healthy brain and a depressed brain. And the exciting thing is, when you treat that depression effectively, the brain goes back to looking like a healthy brain, both at the cellular level and at a global scale. It's critical to understand the neurobiology of depression and how the brain plays a role in that for two main reasons. One, it helps us understand how the disease develops and progresses, and we can start to target treatments based on that. We are in a new era of psychiatry. This is a paradigm shift, away from a model of monoaminergic deficiency to a fuller understanding of the brain as a complex neurochemical organ. All of the research is driven by the imperative to alleviate human suffering. Depression is one of the most substantial contributors to human suffering. The opportunity to make even a tiny dent in that is an incredible opportunity.

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Yale is a great place for multidisciplinary investigations. We have a launch pad to bring many labs together. I think we’re well positioned to make a difference by approaching neurodegeneration and repair from multiple perspectives, taking genetic and pathologic data, designing therapeutics, and ultimately making a clinical impact.

Stephen Strittmatter, MD, PhD

Synapse concentration has widely been touted as the pathologic feature that correlates best with cognitive performance in Alzheimer’s disease. If we are able to validly measure synapse concentrations in living people, then there are enormous implications for therapeutic trials.

Christopher van Dyck, MD

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