Neuroscience
From Neurons to Habits
A neurologist’s science-based guide to caring for the one organ we can’t replace.
Posted December 30, 2025 Reviewed by Margaret Foley
Key points
- Brain health is body health—and the brain is the one organ we cannot replace.
- As we age, neurons are lost through vascular injury and proteinopathy—protein buildup inside cells.
- Exercise, sleep, and diet can slow brain cell loss, both from vascular damage and proteinopathy.
- The right remedy is not always easy. Consistency in daily habits matters more than perfection or quick fixes.
Happy New Year!
Let us begin the new year with a renewed commitment to protecting our brain health.
We often hear that the mind and body are connected—and this is absolutely true. Brain health is body health.
Thanks to remarkable advances in science and medicine, humans now live longer than at any other time in history. We have learned to control infections, reduce deaths from heart disease, and cure or manage many cancers. We can replace worn joints, transfuse blood, implant new lenses in the eyes, and sometimes even transplant kidneys or livers.
But there is one organ that cannot be replaced: the brain.
Brain cells—called neurons—have a unique and sobering property. For the most part, they do not regenerate. We are born with billions of neurons, and once they die, they are gone. Every day, we have slightly fewer neurons than the day before. This is very different from blood cells, bone cells, or liver cells, which continuously regenerate. Simply put: The longer we live, the fewer brain cells we have. That is a biological fact.
This does not mean we should despair.
Neurons have an extraordinary ability to adapt by forming new connections—a property known as plasticity. This is the foundation of learning and compensation, and much of my writing has focused on this hopeful aspect of the brain. Today, however, I want to focus on a more “neuroscience-heavy” question:
What causes brain cells to degenerate and die—and how can we slow that process?
If we can minimize neuronal loss, that is clearly a good thing. And understanding how neurons die is the first step toward protecting them.
Many conditions can damage brain cells—this is essentially the entire field of neurology, my discipline. But as we age, two broad processes dominate:
- Vascular injury
- Neurodegeneration, involving mechanisms such as proteinopathy, energy failure, and inflammation
Let’s briefly discuss the first, because the remainder of this post will focus on the second.
Vascular Injury: Blood Supply Matters
All cells—including neurons—require a steady blood supply to survive. Blood delivers oxygen, glucose, and other essential nutrients. When blood vessels become damaged or narrowed—due to high blood pressure, high cholesterol, diabetes, smoking, dehydration, or simply aging—neurons can become chronically undernourished and eventually die.
When this happens suddenly or in a large area, we call it a stroke. But even without obvious symptoms, small numbers of neurons can die silently over time due to vascular injury. On brain MRI scans, this often appears as “white matter changes” or “small vessel disease”—sometimes referred to as “mini-strokes.”
The message here is straightforward and universal: controlling blood pressure, cholesterol, diabetes, smoking, hydration, and physical activity matters—for the brain as much as for the heart.
Neurodegeneration: When Brain Cells Fail From Within
In contrast to vascular injury, neurodegeneration often occurs silently, without an obvious event such as a blocked blood vessel. While the full process is not yet completely understood—and is likely multifactorial—research over the past 20 years has made enormous progress.
Energy failure at the level of the cell’s power plants (the mitochondria) and chronic inflammation both appear to play important roles. Here, however, I want to highlight one particularly critical process: proteinopathy.
Every cell—including neurons—has a proteostatic network. It is constantly producing proteins and enzymes that carry out essential functions. You can think of a cell as a protein-making factory, and it has a system that maintains the balance of these proteins.
- DNA provides the instructions—the blueprint—for building proteins, through a complex molecular process involving messenger RNA and precise matching of amino acids. Most of the time, this process works beautifully.
- Occasionally, defective proteins are produced. Normally, cells have efficient systems to recognize and dispose of these faulty proteins.
- However, some defective proteins fold into abnormal three-dimensional shapes that make them resistant to breakdown. These proteins accumulate inside the cell, disrupt normal function, and eventually lead to cell death.
Why does this happen?
- Sometimes the original DNA instructions are altered—due to inherited genetic variants or changes that occur over time (so-called epigenetic changes).
- Other downstream cellular processes may also break down. Chance likely plays a role as well: We are part of a biological system, not a precision-engineered robot, and any complex system is inherently prone to occasional errors.
- Other times, the problem lies in the cell’s cleanup machinery, which becomes less efficient with age.
Different neurological diseases involve different proteins, but the underlying mechanism is remarkably similar:
- In Alzheimer’s disease: amyloid and tau
- In Parkinson’s disease: alpha-synuclein
- In other conditions: proteins such as TDP-43, huntingtin, or other forms of tau
Once these protein aggregates form, they can promote further aggregation and, in some cases, spread from one neuron to another—creating a vicious, self-accelerating cycle.
While recent immunotherapies for Alzheimer’s disease have begun to slow this process, and many treatments are currently in clinical trials, we do not yet have a cure. Still, understanding these biological mechanisms represents enormous progress. And importantly, while we currently have limited medications that directly target proteinopathy, everyday lifestyle factors appear to have a major impact on whether this process is minimized or accelerated.
So What Can We Do?
Here are three evidence-based ways to help protect brain health and slow neuronal damage.
1. Exercise
Exercise benefits the brain in multiple ways: It improves blood flow, reduces inflammation, and enhances neurotransmitter and hormone signaling. Multiple studies have shown that (through yet incompletely understood mechanisms), exercise slows down the progression of neurodegenerative disease and brain atrophy. Recent research suggests that a protein released from muscles during exercise—called irisin (discussed in Psychology Today by Christopher Bergland)—may help accelerate the clearance of toxic protein aggregates from the brain. Movement truly is medicine.
2. Sleep
Sleep is not passive downtime—it is an active maintenance period for the brain. During sleep, the brain’s waste-clearing systems (glymphatic system) may become more active, helping remove metabolic by-products and toxins.
Sleep apnea has emerged as a major risk factor for poor brain health. Repeated drops in oxygen levels during sleep are harmful to neurons. For this reason, sleep apnea should be aggressively screened and treated.
3. Diet
There is no single “magic” food or supplement for brain health. Instead, focus on a balanced, nutritious diet—such as a Mediterranean-style diet rich in vegetables, legumes, healthy proteins, and whole foods.
A few important points:
- Most Americans are not deficient in nutrients—we suffer from excess. Sugar and highly processed foods are harmful to the brain and should be minimized.
- Prevent constipation. The gut–brain axis is real: Gut bacteria and intestinal inflammation influence brain health. Some protein aggregates may even begin in the gut and travel to the brain. While we don’t yet know which probiotics are best, a fiber-rich diet and regular bowel habits matter.
- Alcohol: While moderate alcohol may have social or relaxing effects, chronic alcohol exposure is neurotoxic and kills brain cells and peripheral nerves.
These are tried-and-true recommendations—the kind your grandmother may have given you. They are not flashy, novel, or attention-grabbing. But what is simple, right, and hiding in plain sight is often the hardest to do consistently.
You don’t need perfection.
You need consistency.
Small daily habits, practiced over time, are how we protect the one organ we cannot replace.
References
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Nedergaard M, Goldman SA. Glymphatic failure as a final common pathway to dementia. Science. 2020 Oct 2;370(6512):50-56. doi: 10.1126/science.abb8739. PMID: 33004510; PMCID: PMC8186542.
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Xiang J, Tang J, Kang F, Ye J, Cui Y, Zhang Z, Wang J, Wu S, Ye K. Gut-induced alpha-Synuclein and Tau propagation initiate Parkinson's and Alzheimer's disease co-pathology and behavior impairments. Neuron. 2024 Nov 6;112(21):3585-3601.e5. doi: 10.1016/j.neuron.2024.08.003. Epub 2024 Sep 5. Erratum in: Neuron. 2025 Oct 1;113(19):3300-3302. doi: 10.1016/j.neuron.2025.09.015. PMID: 39241780.

