A new study, published on June 23 in Nature Communications Earth & Environment, analyzed water quality in more than 500 watersheds across the Western U.S., and is the first large-scale assessment of post-wildfire quality.

The research was led by scientists from the Cooperative Institute for Research in Environmental Science (CIRES) at the University of Colorado Boulder.

“We were attempting to look at notable trends in post-wildfire water quality across the entire U.S. West, to help inform water management strategies in preparing for wildfire effects,” said Carli Brucker, lead author and former CU Boulder and Western Water Assessment PhD student.

The results showed contaminants like organic carbon, phosphorus, nitrogen, and sediment can degrade water quality for up to eight years after a fire. Water managers can use this data to help them plan for the future and respond appropriately when wildfires strike.

CIRES Fellow and Western Water Assessment Director Ben Livneh was the principal investigator and co-author of the study. Much of his research focuses on hydrology, or water supply, on a continental scale. When he realized he could use the same approach to understand large-scale trends in water quality, he was excited to test the method.

“There’s been a lot of work, for example, in the National Climate Assessment and the International Panel on Climate Change talking about changes in global water supply,” said Livneh, associate professor in the Department of Civil, Environmental and Architectural Engineering. “But those assessments point to this gap in water quality assessments in a continental scale context, whereas people like me in physical hydrology have been thinking about the continental scale challenges for a while.”

Researchers have long known that fire ash and soil destruction contribute to degraded water quality. Yet, past research has largely been limited to state and municipal studies — cities and towns test water quality in local streams and rivers following large fires.

For the new study, the team analyzed more than 100,000 water samples from 500 sites: half from burned river basins and half from unburned. They measured levels of organic carbon, nitrogen, phosphorus, and sediment as well as turbidity, or cloudiness, of each sample.

To understand wildfire-driven impacts, the team built data-driven models to measure how much contaminants changed in each basin before and after wildfires. In the final step, they compiled data to find the average across the burned basins for each pre- and post-wildfire year, and then compared those to the unburned basins.

The results showed watersheds take longer to recover after wildfires than previous studies found. Organic carbon, phosphorus, and turbidity are significantly elevated in the first one to five years post-fire. Nitrogen and sediment show significant increases up to eight years post-fire. Fire-driven impacts were worse in more forested areas.

“It can take two years, up to eight years, for the effect to be fully felt,” Livneh said. “Sometimes it can be a delayed effect, meaning, it’s not all happening right away, or sometimes you need a big enough storm that will mobilize enough of the leftover contaminants.”

Each watershed in the study felt the impacts differently. This is likely tied to where the fire struck — a fire closer to the river would be worse than an upstream fire. Different soils, vegetation, and weather also change the impact in each watershed, making it difficult to plan for the future.

“There’s a huge amount of variability in sedimentation rates,” said Brucker, who now works as a consultant. “Some streams are completely clear of sediment after wildfires, and some have 2000 times the amount of sediment.”

Despite variability across river basins, the study provides concrete numbers that give insight to water managers across the Western U.S. Researchers hope the results provide better direction on informing future planning efforts for increasing wildfire resilience.

“I’m hoping that providing concrete numbers is very impactful to water managers,” Brucker said. “You can’t fund resilience improvements on general concerns alone. Water managers need real numbers for planning, and that’s what we’re providing,” Brucker said.

Microglial cells, the resident immune cells of the central nervous system (CNS), regulate inflammatory responses by releasing pro-inflammatory cytokines — chemical signaling molecules. While the neuroinflammatory functions of microglial cells are well-documented, the exact role of astrocytes (a specialized type of glial cell) in neural growth and development has remained unclear until recently. To shine light on the role of astrocytes in neuroinflammation and in the pathophysiology of MDD, a team of researchers, led by Dr. Gaurav Singhal from the Department of Surgery, University of Wisconsin, USA, conducted an in-depth review of literature. Their findings will be published in Neuroprotection.

Explaining the motivation behind the present study, Dr. Singhal says, “MDD is one of the leading causes of disability worldwide and affects more than 280 million people across all age groups and regions. Moreover, the economic burden of MDD is substantial, with annual costs in the United States alone exceeding $326 billion. Gaining insights into the role of astrocytes in neuroinflammation can aid the development of therapeutic approaches to treat depression and other psychiatric disorders.”

The research team began by conducting a comprehensive literature search using widely used online repositories such as PubMed and Google Scholar. They evaluated 226 research papers relevant to astrocytes, neuroinflammation, and depression. To ensure the high quality of their study, they followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.

In their analysis, the researchers found that astrocytes were key to maintaining the structural integrity of synaptic junctions between neurons. The release of neurotrophic factors such as brain-derived neurotrophic factor and fibroblast growth factor-2 by astrocytes were critical for the promotion of neurite growth and synapse formation. Besides stabilizing the tripartite synapse comprising of neuron-astrocyte-neuron, astrocytes further facilitated the effective communication between neurons via regulation of the ionic environment. Notably, changes in astrocyte morphology and function were associated with poor synaptic connectivity, contributing to the development of depressive symptoms.

Furthermore, they discovered a critical mechanism involving activated microglia and astrocytes that resulted in sustained neuroinflammation in MDD. The first step of the mechanism was the release of pro-inflammatory cytokines like tumor necrosis factor-α and interleukin-1 from activated microglia cells. These signals subsequently induced the secretion of additional inflammatory chemicals from astrocytes, thereby amplifying neuroinflammation.

Elaborating on the molecular crosstalk between microglia and astrocytes during MDD, Dr. Singhal explains, “Increased intracellular calcium levels within astrocytes can induce the release of adenosine triphosphate (ATP), which, in turn, triggers a delayed calcium response in microglial cells. Following multiple cycles of astrocyte-released ATP-based activation,  microglial cells eventually undergo apoptosis or programed cell death.”

Additionally, preclinical studies involving murine models showed that astrocytic lactate dehydrogenase A enzyme, responsible for lactate production, is important for maintaining neuronal excitability. A process known as histone lactylation — where lactate molecules are added to histone proteins in DNA — was found to alter gene expression, thereby contributing to astrocyte-driven neuroinflammation.

Taken together, this study highlights the molecular mechanisms underlying astrocytic dysfunction, wherein astrocytes switch from a neuroprotective role to one that promotes neuroinflammation by increasing the expression and secretion of inflammatory cytokines.

Alzheimer’s disease affects millions of people around the world and occurs when abnormal proteins build up in the brain, leading to the death of brain cells and declines in cognitive function and memory. While current treatments can manage symptoms of Alzheimer’s, the new gene therapy aims to halt or even reverse disease progression.

Studying mice, the researchers found that delivering the treatment at the symptomatic stage of the disease preserved hippocampal-dependent memory, a critical aspect of cognitive function that is often impaired in Alzheimer’s patients. Compared to healthy mice of the same age, the treated mice also had a similar pattern of gene expression, suggesting that the treatment has the potential to alter the behavior of diseased cells to restore them to a healthier state.

While further studies will be required to translate these findings into human clinical trials, the gene therapy offers a unique and promising approach to mitigating cognitive decline and promoting brain health.

The study, published in Signal Transduction and Targeted Therapy, was led by senior author Brian Head, Ph.D., professor of anesthesiology at UC San Diego School of Medicine and Veterans Affairs research career scientist, and co-senior author Shanshan Wang, M.D. Ph.D., an assistant professor of anesthesiology at UC San Diego School of Medicine. The gene therapy technology was licensed by UC San Diego to Eikonoklastes Therapeutics in 2021. Eikonoklastes was granted Orphan Drug Designation (ODD) by the FDA for the use of the patented gene therapy in amyotrophic lateral sclerosis (ALS) also known as Lou Gehrig’s disease.