In my work as a computational neuroscientist, I study how networks emerge, organize, and fail. From neural circuits to social systems, network architecture determines function. But there's a network story I've been reluctant to tell because it sits in a controversial space: the neurotoxic effects of indoor mold exposure, specifically from Stachybotrys chartarum, commonly known as black mold.
Although there has been recent research (2024-2025) providing mounting evidence for mycotoxin-induced neurotoxicity, there still has been quite the controversy around this topic. The controversy around mold toxicity is largely social: people who report cognitive symptoms from water-damaged buildings are often dismissed, however, this is an evolving field of inquiry that will hopefully elucidate better mechanisms as time goes by. Understanding the network dynamics at play, both in fungal growth and in neural disruption, might help legitimize these experiences while grounding them in rigorous science.
Full disclosure: my own health problems, immune sensitivities, and chronic exposure to black mold throughout my graduate education (Master's and Doctoral studies) over 10 years, and a recent health attack led me to realize the full extent of this problem.
Fungal Networks as Adaptive Systems
Before we discuss disruption, we need to understand what we're dealing with. Fungi don't grow like plants or bacteria. They develop as interconnected networks of thread-like hyphae that branch, fuse, and reorganize in response to resource availability. These mycelial networks solve optimization problems in real-time: finding food sources, transporting nutrients across distances up to several meters, and adapting their architecture based on damage or opportunity.
Stachybotrys chartarum belongs to this class of network-forming organisms. It thrives on cellulose-rich materials like drywall and wallpaper in water-damaged buildings. Unlike faster-growing molds, S. chartarum is a slow colonizer, but it excels in environments with constant moisture, large temperature fluctuations, and minimal competition.
Mechanisms of Mycotoxin Neurotoxicity
The neuroscience literature on mycotoxins has exploded in recent years. A 2025 scoping review by Abia et al. identified multiple pathways through which common mycotoxins, including those from S. chartarum, induce neurotoxicity. The mechanisms read like a catalogue of neural network failure modes.
First, oxidative stress and neuroinflammation. Mycotoxins like aflatoxin B1, ochratoxin A, and trichothecenes increase reactive oxygen species in neuronal cells, triggering pro-inflammatory cascades. Elevated levels of IL-1β, IL-6, and TNF-α create a neuroinflammatory environment that disrupts normal synaptic function.
Second, mitochondrial dysfunction. Impaired mitochondrial function means energy deficits in neurons, leading to apoptosis in vulnerable populations like olfactory sensory neurons.
Third, neurotransmitter dysregulation. Multiple studies document alterations in serotonin, dopamine, and GABA systems following mycotoxin exposure. The clinical manifestations align with what people report: mood changes, cognitive impairment, memory deficits, brain fog, anxiety, and depression.
Neural Networks as Vulnerable Architectures
Mycotoxin-induced neuroinflammation represents diffuse, metabolic attack. It doesn't need to kill specific neurons. It degrades the support infrastructure: astrocytes, microglia, vascular endothelial cells, and mitochondria. The result is a network that remains structurally intact but functionally compromised.
The symptoms people describe align perfectly with this model: brain fog, concentration problems, memory issues, mental fatigue, and difficulty with executive function. These aren't vague complaints, but the expected output of a neural network operating under metabolic constraint and chronic low-grade inflammation.