Research Expertise and Interest

neuroscience, aging, dementia, stress, neural stem cells, epilepsy, traumatic brain injury, blood brain barrier, prosocial behavior

Research Description

The overall goal of my research program is to conduct interdisciplinary multilevel research addressing fundamental questions about brain function with direct relevance to the human condition.  To do that I adopt an integrative systems level approach to brain research which translates across multiple levels of analysis- genomics, molecular, cellular, physiological, systems and behavioral.

Specifically, a major project aims at studying the effects of early life stress on crating vulnerability to mental disease throughout life, with a focus on regulation and functional relevance of adult hippocampal stem cells. In this project we investigate the function of the newborn neurons and their integration into the existing circuitry of learning, memory and emotional processing. Additionally, we aim to determine the environmental and internal cues that control the state and fate choices (neurons vs. glia) of adult hippocampal stem cells, and the role of gene expression and RNA processing (i.e., transcription regulation, RNA splicing and micro RNA), in the translation of those cues to fate decisions made by the stem cell.

A second project aims at studying the mechanisms of epileptogenesis that follow traumatic brain injury and precede the onset of clinical epilepsy. We demonstrated that disruption of the blood-brain barrier (BBB), as occurs after head injury, is a major precipitating event in triggering epileptogenesis. Using rodent models, we have shown that albumin, a major component of the blood, enters the brain during BBB dysfunction, and activates the TGF-β signaling pathway in astrocytes, triggering a regulatory cascade that modulates inflammation and neuroexcitability. Critically, we have shown that blocking albumin from binding to and activating the TGF-β receptor prevents subsequent epileptiform activity and onset of spontaneous seizures. We are currently investigating the mechanistic details by which TGF-β signaling contributes to epileptogenesis, via its affects on adult neural stem cells, neurons and glia, as well as translating our findings towards the clinical context by investigating the efficacy of drugs that block the TGF-β receptor.

In the News

Anxiety and PTSD linked to increased myelin in brain

A recent study links anxiety behavior in rats, as well as post traumatic stress disorder (PTSD) in military veterans, to increased myelin — a substance that expedites communication between neurons — in areas of the brain associated with emotions and memory.

Rats prefer to help their own kind. Humans may be similarly wired

A decade after scientists discovered that lab rats will rescue a fellow rat in distress, but not a rat they consider an outsider, new UC Berkeley research pinpoints the brain regions that drive rats to prioritize their nearest and dearest in times of crisis. It also suggests humans may share the same neural bias.

Drugs that quell brain inflammation reverse dementia

Drugs that tamp down inflammation in the brain could slow or even reverse the cognitive decline that comes with age. In a publication appearing today in the journal Science Translational Medicine, University of California, Berkeley, and Ben-Gurion University scientists report that senile mice given one such drug had fewer signs of brain inflammation and were better able to learn new tasks, becoming almost as adept as mice half their age.

Bromances may be good for men’s health

Male friendships, portrayed and often winked at in bromance movies, could have healthful effects similar to those seen in romantic relationships, especially when dealing with stress.

Seizing Control of Brain Seizures

Daniela Kaufer made a startling discovery about the effect of psychological stress on the brain a few years after serving in the Israeli army during the first Gulf War. 

New neurons help us to remember fear

UC Berkeley’s Daniela Kaufer and colleagues have discovered one way by which emotions such as fear affect memory. The brain’s emotional center, the amygdala, induces the hippocampus, a relay hub for memory, to generate new neurons. In a fearful situation, these newborn neurons are activated by the amygdala, providing a “blank slate” for the new fearful memory.

Featured in the Media

Please note: The views and opinions expressed in these articles are those of the authors and do not necessarily reflect the official policy or positions of UC Berkeley.
February 18, 2022
Allen Martin and Molly McCrea
A group of Bay Area scientists have unraveled some surprising secrets about post-traumatic stress disorder or PTSD which one day could lead to better therapies and treatments. At UC Berkeley, neuroscientist Dr. Daniela Kaufer and now UCSF post-doc Kimberly Long — along with UCSF and San Francisco scientists Radiologist Dr. Linda Chao and Psychiatrist Dr. Thomas Neylan — may have provided a convincing reason why some people are resilient to trauma and others are susceptible. According to statistics, 70 percent of American adults experience at least one traumatic event in a lifetime. Twenty percent of those will develop PTSD, and their symptoms vary dramatically. In their research, the scientists made two important discoveries: that anxiety and traumatic stress are linked to increased myelin in a part of the brain where there is less myelin; and that where the increased myelin is found correlates to the particular symptom. For more on this, see our story at Berkeley News.
December 5, 2019
Drugs that reduce inflammation in the brain may be able to slow or reverse age-related dementia, a team of Berkeley researchers has found. The work promises not only potential treatments for cognitive decline but also surprising new insights into what causes dementia. "I think we're showing a new way to explain very early stages of decline in the brain, and some of it, interestingly, is decline in the normal aging brain, and that's something that we really know very, very little about, or that we knew almost nothing about before we looked at it," says integrative biology professor Daniela Kaufer, the study's senior author. "We're offering a new way to look at it, and the answer came from sort of an unexpected angle. You would think that it would be the cells -- the neurons, the nerve cells, but actually the real secret was in the blood vessels in the brain. ... What we found is dysfunction of the blood-brain barrier that increases in age, and we documented it in rodents and in humans." Link to audio. For more on this, see our press release at Berkeley News. Other stories on this topic appeared in the Daily Mail (UK), Technology.org, New Atlas, MindBodyGreen, and Henri Le Chat Noir.
November 20, 2019
Amy Fleming
Stress has got such a bad rap, says integrative biology professor Daniela Kaufer of Berkeley's Helen Wills Neuroscience Institute. "There's this perception that stress is always bad for the brain, but that's not true. Your stress response is crucial to your survival. It elevates your performance, is super-important for alertness and prepares you to adapt to the next thing that comes along." The type of stress she's referring to here is known as eustress, and through research she and her team have found physiological evidence of its power. Comparing activity in the hippocampuses of rats exposed to prolonged stress as opposed to moderate stress that's comparable to eustress in humans, they found that the lesser stress triggered the growth of new neurons. "Those neurons, we were able to show, are then activated selectively and help in learning for the next situation that is stressful. So you're performing better in that moment, and then you are better equipped for future stressors."
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