Same age, different cognitive trajectory
Why do two patients of the same age not age the same way cognitively? That was the opening question of the Simplycure webinar of 27 October 2026, led by Pauline Chambon, Doctor of Pharmacy and head of training at Dynveo. She first set out the scale of the issue: 57 million people worldwide live with a significant deficit in cognitive function today, and that figure is expected to triple by 2050 as the population ages.
The brain is a demanding organ. It accounts for around 2% of body mass but uses around 20% of the body's energy, 20% of its oxygen and 25% of its glucose. Yet it has few energy reserves: it runs on a just-in-time basis, constantly dependent on its supply of oxygen, glucose and micronutrients. For Pauline Chambon, brain ageing does not mean inevitable cognitive decline: the vulnerability of the ageing brain shows up very differently from one person to the next.
Cognitive reserve, a safety cushion that can be strengthened
Biological markers of brain ageing, such as amyloid plaques, do not directly predict cognitive performance. According to the data Pauline Chambon cited, 20 to 30% of people aged 60 to 75 show amyloid markers without measurable cognitive decline. What makes the difference is cognitive reserve: a safety cushion that lets the brain absorb insults before problems become clinically visible. It does not slow ageing down, it compensates for its effects.
Behind the term, Pauline Chambon distinguishes two dimensions, which together form cognitive resilience:
- Brain reserve, meaning quantity: brain volume, number of neurons and synapses, density of the vascular network.
- Cognitive reserve, meaning quality: transmission speed, connections between brain regions, synaptic plasticity.
The good news, in her view: this reserve is not a fixed capital that gets used up. It can be maintained and strengthened throughout life, including through cognitive activity later on, after 60. The study she presented associates a high cognitive reserve with a 47% lower frequency of cognitive decline. The levers cited: intellectual stimulation (learning, reading, staying curious), sleep (the glymphatic system cleans the brain during deep sleep, and REM sleep consolidates long-term memory), physical activity for cerebral microcirculation, social connection, often underestimated even though an interaction draws on memory, attention and language, and finally the plate, complemented by supplements where needed.
The four drivers of brain ageing
Pauline Chambon describes four biological mechanisms that add up and feed one another:
- Mitochondrial dysfunction: a neuron contains 1,000 to 2,000 mitochondria. With age, they produce less energy and more free radicals, and mitophagy, their quality control, works less well.
- Oxidative stress: the brain is particularly exposed, because it uses a lot of oxygen, it is very rich in polyunsaturated fatty acids that are sensitive to oxidation, and it has few endogenous antioxidant defences.
- Inflammaging: low-grade background inflammation linked to ageing. The microglia, the brain's immune cells, move into a so-called primed state and react to the slightest stimulus, with increased production of pro-inflammatory cytokines (IL-6, interleukin-1 beta, TNF alpha).
- Vascular dysfunction: the tight junctions of the blood-brain barrier lose quality, the barrier lets through what should not get in, and glymphatic clearance becomes less efficient.
She adds a fifth player, not a driver of ageing but a key target: acetylcholine, the neurotransmitter of memory, attention and information encoding. Synthesised from choline and acetyl-CoA, it is broken down by acetylcholinesterase and then recycled. Several of the options presented act on this cycle.
Case 1: brain fog in her fifties
Sophie, 50, a marketing director, comes in for brain fog that has set in over eight months: trouble concentrating in meetings, words on the tip of her tongue, cognitive fatigue and irritability at the end of the day. She sleeps six hours a night with awakenings, moves little and eats on the go. Her initial check-up is normal.
First of all, Pauline Chambon draws attention to hormonal status: in a woman aged 40 to 50 who reports brain fog, perimenopause is a turning point in female brain ageing. Oestradiol stimulates BDNF and modulates dopamine and serotonin, and 80% of women going through the menopause transition report cognitive disturbances. Here, she settles on a picture of cerebral overload linked to stress and mental load, and three lines of action:
- An adaptogen, rhodiola, which helps restore negative feedback on cortisol and supports energy at mitochondrial level, hence its value for stress-induced fatigue. It is taken in the first part of the day, because of its stimulating effect. Quality benchmark cited: standardisation at 5% rosavins and 2% salidroside, where extracts at 3% and 1% are common on the market.
- Magnesium L-threonate, for neuronal excitability and synaptic plasticity. Threonate, a vitamin C derivative close to glucose, lets it use glucose transporters and cross the blood-brain barrier better than other forms of magnesium. It modulates NMDA receptors, which are involved in learning. According to Pauline Chambon, it is the form to choose whenever cognitive function is the goal, with an evening dose, ideally one hour before bed.
- Omega-3s, favouring DHA: neuronal membranes are 60% lipids, a third of which is DHA, and nine people in ten do not consume enough omega-3s. They support membrane fluidity, are precursors of molecules that take part in resolving inflammation, and favour BDNF activity. They are taken with a fatty meal, for at least 12 weeks, the time it takes to remodel membranes. Quality criteria cited: a triglyceride form and a Totox index below 10.
A useful marker: the omega-3 index, the ratio of EPA + DHA to total fatty acids measured on the red blood cell fatty acid profile. It reflects intake over the previous three months and should be 8% or higher.
Case 2: a memory complaint with a hippocampal profile
Jean-Pierre, 68, a retired teacher, looks after his cognitive reserve well: bridge, reading, crosswords, a varied diet, 30 minutes of walking a day. Yet he forgets proper names, repeats the same stories, misplaces things and loses the thread of what he reads, signs confirmed by his wife. He remains independent, and his neuropsychological assessment shows an isolated deficit in episodic memory: a hippocampal profile. The only finding on his blood test is homocysteine at 13.5.
Two targets, according to Pauline Chambon. First, cholinergic signalling:
- Citicoline (CDP-choline) splits into choline, a precursor of acetylcholine, and cytidine, which takes part in the synthesis of phosphatidylcholine in neuronal membranes. Its stated advantage: oral bioavailability of around 90%. Pauline Chambon stresses this point, because poorly absorbed choline stays in the intestinal lumen, where the microbiota and then the liver convert it into TMAO, which is harmful at vascular level.
- Huperzine A, extracted from a club moss, Huperzia serrata, interacts with acetylcholinesterase and extends the lifespan of acetylcholine in the synaptic cleft. In the study presented, conducted in around a hundred people over one month with 150 micrograms twice a day, 74% of participants showed a favourable change in memory and overall cognitive function, compared with 40% on placebo.
Next, homocysteine metabolism. This transitional amino acid, a product of methylation reactions, should be remethylated into methionine with vitamins B9 and B12, or transsulfurated into cysteine with B6. When it accumulates, it weighs on cognitive function and on the cardiovascular picture. B12 deficiency is common with age: fewer animal products, dentition, declining appetite, medicines that disrupt its absorption. Pauline Chambon cites the VITACOG trial, run over two years: taking B vitamins reduced homocysteinaemia by 22.5%, while it rose in the placebo group, with stabilisation of executive function. She favours a complex of the eight B vitamins in bioactive form, for example B9 as 5-methyltetrahydrofolate.
Case 3: cognitive slowing with a cardiovascular background
Michel, 72, a former accountant, widowed, lives alone and remains independent. He has had high blood pressure for around fifteen years, a lipid imbalance, slight excess weight and little physical activity. He comes in for cognitive slowing: he takes longer to understand, switches off when several tasks arrive at once, and struggles to plan. His memory for events is relatively preserved. For Pauline Chambon, this picture is typical: with an unfavourable cardiovascular background, cerebral vascular dysfunction is likely, and executive functions are the first to be affected.
- Ginkgo biloba supports cerebral microcirculation, acts on blood viscosity and has antioxidant activity. Precautions cited: it is not recommended for someone on anticoagulants, and it should be stopped at least four days before surgery.
- Curcumin, because what is needed is an antioxidant able to cross the blood-brain barrier, which is rare. It also stimulates BDNF. In the study presented, conducted in 40 subjects over eighteen months with 90 mg twice a day, it improved visual memory, attention and verbal memory. Its natural limitation is intestinal absorption: a micro-encapsulated form improves its solubility, and part of it escapes hepatic glucuronidation. It is taken with a main meal and, it too, is not recommended alongside anticoagulant therapy.
Which markers to monitor routinely?
Asked during the Q&A, Pauline Chambon cited homocysteine, to be measured directly, vitamin B12, iron, which matters for all cognitive functions, vitamin D and, for those who want a precise indicator, the omega-3 index. She points out that test results are always read alongside symptoms. On iron, she considers that adding vitamin C is not necessary with a well-absorbed form such as iron bisglycinate, whereas it helps with non-haem iron from food.
Watch the webinar
The full replay (in French) is available below, with chapters. The Q&A also covers activated B vitamins, combining ginkgo with an antiplatelet medicine, cortisol regulation by rhodiola, appetite in older adults and whether the same reasoning applies to younger patients.
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