Daniela Kaufer

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.