Definition & diagnostic criteria

Mild NCD is characterised by a modest decline in one or more cognitive domains (memory, attention, executive function, language, visuospatial skills) that is greater than expected for age and education, but does not substantially impair independence in daily activities—though greater effort or compensatory strategies may be needed.

Common subtypes & causes

• Amnestic MCI (single or multiple domain): predominant memory deficits — higher risk of progression to Alzheimer’s disease.
• Non-amnestic MCI: deficits in attention, language, or visuospatial function — may progress to other dementias (FTD, DLB, vascular).
• Vascular mild NCD: small vessel disease or prior stroke causing executive dysfunction and slowed processing.
• Substance/medication-related: anticholinergics, sedatives, alcohol effects.
• Metabolic & endocrine: hypothyroidism, B12 deficiency, uncontrolled diabetes.
• Depressive pseudodementia / psychiatric contributors: cognitive complaints related to mood disorders.

Symptoms — what patients often report

• Subjective memory complaints — forgetting recent conversations or appointments.
• Difficulty multitasking, slower thinking and reduced concentration.
• Word-finding difficulties and reduced verbal fluency.
• Visuospatial challenges — trouble navigating or judging distances.
• Occasional mood changes, apathy or anxiety related to awareness of decline.

Assessment — practical approach

1. Obtain collateral history to confirm decline and assess impact on function.
2. Use sensitive cognitive screening tools (MoCA recommended over MMSE for MCI detection).
3. Perform focused neuropsychological testing when subtype clarification or baseline measurement is needed.
4. Comprehensive medication review to identify iatrogenic contributors (anticholinergics, benzodiazepines).
5. Screen for depression, sleep disorders and substance use.
6. Assess vascular risk factors and functional status (IADLs).

Investigations — essential and targeted

• Baseline blood tests: CBC, electrolytes, renal and liver function, glucose, TSH, B12, folate.
• Neuroimaging: MRI brain to detect atrophy patterns, small vessel disease or structural lesions.
• Consider sleep study if sleep apnoea suspected; toxicology when substance use is possible.
• Optional biomarkers: CSF amyloid/tau or PET imaging in select cases where early Alzheimer’s pathology confirmation may influence management.

Treatment & management strategies

There are no universally approved medications to reverse MCI. Management focuses on identifying and treating reversible causes, risk reduction, cognitive and functional support, and monitoring for progression.

Address reversible causes

• Correct vitamin deficiencies, thyroid dysfunction, and optimise glycaemic control.
• Deprescribe anticholinergic and sedative medications where safe.
• Treat sleep disorders and substance misuse.

Lifestyle & risk reduction

• Vascular risk control: manage hypertension, lipids, diabetes and smoking cessation.
• Regular physical exercise, Mediterranean-style diet, cognitive engagement and social activity.
• Manage hearing loss and vision impairment to reduce cognitive load.

Cognitive interventions

• Cognitive training and rehabilitation tailored to domains of weakness.
• Cognitive stimulation groups and structured activities to support memory and executive function.

Pharmacological considerations

• No routine recommendation for cholinesterase inhibitors or memantine for MCI—consider only in specialist settings or clinical trials.
• Treat comorbid mood/anxiety disorders (SSRIs) which may improve cognitive complaints.

Key takeaways

• Mild NCD is an early, potentially modifiable stage—identify reversible causes and optimise vascular and lifestyle risk factors.
• Use sensitive screening (MoCA) and consider neuropsychology for baseline profiling.
• Non-pharmacological interventions (exercise, cognitive training) and deprescribing are cornerstone strategies.
• Regular follow-up and caregiver education are essential to monitor progression and plan care.