Brain Health Basics
You have roughly 86 billion of them. They define your memories, your personality, your sense of self. Here's what neurons actually are, and why protecting them is essential.
There is a moment in Alzheimer's disease that many families know: a loved one fails to recognise a face they have seen a thousand times, or loses the thread of a sentence mid-way through speaking it. It feels abstract, even mysterious — our psyches are complex. But at the biological level, what is happening is concrete and specific. Neurons are dying.
Understanding what neurons are, and what makes them vulnerable, is the first step to understanding what Alzheimer's disease actually does, and why OneCarbon's research is focused on protecting these cells before the damage becomes irreversible.
A neuron is a specialised cell whose job is to transmit information. While your body contains trillions of cells, like skin cells, muscle cells, and blood cells, neurons are unique in their ability to send electrical and chemical signals across vast distances at extraordinary speed. They are, in the most literal sense, the hardware on which your mind runs.
The human brain contains approximately 86 billion neurons, each connected to thousands of others through junctions called synapses. When you recall a memory, feel an emotion, or decide to reach for a glass of water, you are triggering a cascade of signals racing across these connections. Learning, in neurological terms, is the process of strengthening certain connections and weakening others — literally reshaping the physical architecture of your brain.
Most cells in your body are regularly replaced. The cells lining your stomach renew every few days. Your skin replaces itself roughly every month. But neurons are fundamentally different: the vast majority of them are formed before birth and must last a lifetime. While some limited neurogenesis (the creation of new neurons) does occur in adult brains, it cannot come close to compensating for significant neuronal loss.
This is what makes neurodegenerative diseases so devastating. When neurons die in large numbers, the brain simply cannot replace them. The connections they maintained, the memories they encoded, the functions they performed — all of it is lost. Permanently.
Why this matters for Alzheimer's
In Alzheimer's disease, neurons in regions responsible for memory and reasoning are among the first to be affected. The disease typically begins silently with neurons under stress years or even decades before any symptoms emerge. This window of vulnerability, before irreversible loss, is exactly where interventions like OneCarbon's probiotic are designed to act.
Neurons are among the most energy-hungry cells in the human body. The brain accounts for only around 2% of your body weight, yet it consumes roughly 20% of your total energy. This is because maintaining the electrical gradients required for signalling, and sustaining the thousands of synaptic connections each neuron holds, is metabolically expensive work that never stops, even while you sleep.
That energy is produced almost entirely in tiny structures within the cell called mitochondria, which are often described as the cell's power stations. Healthy mitochondrial function is not simply a nice-to-have for neurons; it is an existential requirement. When mitochondrial function declines, as it does in the early stages of Alzheimer's disease, neurons begin to lose the energy they need to maintain their connections, clear toxic proteins, and ultimately survive.
Alzheimer's disease is characterised by the accumulation of two abnormal proteins in the brain: amyloid-beta, which clumps into plaques between neurons, and tau, which forms tangles within them. These aggregates disrupt normal neuronal function and trigger inflammation. But the damage doesn't stop there — they also impair mitochondrial function, cutting off the energy supply neurons depend on.
What our research at the University of Cambridge revealed is that neurons don't simply surrender to this assault. They fight back — specifically, by activating a cellular pathway called one-carbon metabolism, which helps restore mitochondrial function and maintain the energy levels neurons need to remain resilient. Neurons that can sustain this response survive longer; neurons that cannot are more vulnerable to disease progression.
While Alzheimer's is the most common cause of neuronal loss in older adults, it is far from the only one. Neurons are surprisingly vulnerable to a wide range of insults; some dramatic, some mundane, and some that accumulate quietly over decades.
Other neurodegenerative diseases such as Parkinson's, which destroys the dopamine-producing neurons that control movement, and ALS (motor neurone disease), which targets the neurons responsible for voluntary muscle control, operate through distinct but overlapping mechanisms. Mitochondrial dysfunction — the same energy failure that features in Alzheimer's — plays a central role in both.
Stroke is among the most acute causes of neuronal death. When blood flow to a region of the brain is cut off, even briefly, neurons are deprived of the oxygen and glucose they need to function. Because of their exceptional energy demands, they begin to die within minutes — faster than almost any other cell type in the body.
Traumatic brain injury causes both immediate neuronal death from physical damage, and a slower secondary wave of damage in the hours and days that follow, driven by inflammation, oxidative stress, and — again — mitochondrial failure. Repeated mild head trauma, as seen in contact sports, has been linked to a neurodegenerative condition called CTE, which shares some features with Alzheimer's.
Chronic lifestyle factors also take a measurable toll. Heavy alcohol consumption is directly neurotoxic; sustained high blood sugar, as seen in poorly controlled type 2 diabetes, damages the small blood vessels that supply neurons; and chronic sleep deprivation impairs the brain's ability to clear the metabolic waste products that accumulate during waking hours, such as amyloid-beta. Even prolonged psychological stress, through the sustained release of the hormone cortisol, has been shown to damage neurons in the hippocampus, the brain region most associated with memory.
The common thread running through nearly all of these threats is energy failure. Neurons that are metabolically robust — that can generate energy efficiently, manage oxidative stress, and respond flexibly to changing conditions — are better equipped to survive all of them. This is why supporting neuronal metabolism, rather than targeting any single disease mechanism, represents such a promising general strategy for long-term brain health.
The reason this discovery matters is that it points to a window for intervention. By the time someone receives an Alzheimer's diagnosis, substantial neuronal loss has often already occurred. But the stress response, the activation of one-carbon metabolism in struggling neurons, begins much earlier. If we can support and amplify that response, we may be able to keep neurons healthier for longer, slowing or potentially preventing the progression of the disease.
That is precisely the logic behind OneCarbon's probiotic, 1C-01. Rather than targeting the toxic proteins of Alzheimer's after they have formed — the approach of most existing drugs — we are working to strengthen the neuron's own defences by supplying the metabolites it uses to run one-carbon metabolism. Think of it less as treating a fire, and more as fireproofing the building.
We are still gathering the evidence. 1C-01 has not been proven to prevent or treat Alzheimer's disease. But the science behind the approach is robust — and the urgency is real. Every neuron that survives is a memory preserved, a word found, a face recognised.