Cognitive Decline

Cognitive change with age exists on a spectrum. Normal ageing brings slower processing speed and occasional word-finding difficulty without loss of independence. Mild cognitive impairment involves objective deficits on testing that are greater than expected for age but do not compromise daily function; roughly 10-15% of people with MCI progress to dementia each year, and some revert to normal. Dementia is defined by cognitive decline sufficient to impair independent living. The most consequential finding of the last decade is how much of this is potentially preventable. The 2024 Lancet Commission identified fourteen modifiable risk factors accounting for around 45% of dementia cases worldwide: lower education, hearing loss, high LDL cholesterol, depression, traumatic brain injury, physical inactivity, diabetes, smoking, hypertension, obesity, excess alcohol, social isolation, air pollution and untreated vision loss. Hearing loss alone is among the largest single contributors, and hearing aids are one of the more actionable interventions available. Reversible causes should always be excluded before attributing decline to neurodegeneration: B12 deficiency, hypothyroidism, depression, obstructive sleep apnoea, medication effects — particularly anticholinergics and benzodiazepines — and excess alcohol all produce cognitive impairment that improves when addressed. Supplement evidence is weaker than the marketing suggests. B12 correction helps when deficiency is present. Omega-3 shows benefit in observational studies and in some trials in people with mild impairment or APOE4 carriage, but large prevention trials in cognitively healthy older adults have been largely null. Ginkgo has failed in large prevention trials. No supplement has been shown to prevent dementia.

• •Forgetting recent conversations or events
• •Repeating questions
• •Difficulty finding words
• •Losing track of the thread in conversation
• •Trouble with planning, sequencing or managing finances
• •Getting lost in familiar places
• •Reduced initiative or apathy
• •Difficulty with complex tasks previously managed easily
• •Personality or behaviour change

• •Alzheimer disease
• •Vascular cognitive impairment
• •Lewy body dementia
• •Frontotemporal dementia
• •Vitamin B12 deficiency
• •Hypothyroidism
• •Depression, which can mimic dementia
• •Obstructive sleep apnoea
• •Anticholinergic and sedative medications
• •Excess alcohol
• •Untreated hearing loss
• •Uncontrolled hypertension and diabetes

Alzheimer disease involves extracellular amyloid-beta plaque accumulation and intracellular tau neurofibrillary tangles, with synaptic loss preceding overt symptoms by 15-20 years. Vascular contribution is common and frequently coexists — small vessel disease, microinfarcts and reduced cerebral perfusion. Neuroinflammation and microglial activation are increasingly recognised as active participants rather than bystanders. The long preclinical window is precisely why midlife risk factor control, rather than late intervention, offers the most leverage.