ICD-116D71	MILD NEUROCOGNITIVE DISORDER (MCI) Mild neurocognitive disorder
ICD-10F06.7	Mild cognitive disorder
DSM-5-TRG31.84	Mild Neurocognitive Disorder

1. Definition and nosology

Mild Neurocognitive Impairment (ICD-11: 6D71 Mild Neurocognitive Disorder; DSM-5-TR: G31.84) — mild decline in one or more cognitive domains (memory, complex attention, executive function, language, visuospatial, social cognition); Daily activity is maintained (though compensation may be needed). Typical name — “Mild Cognitive Impairment” (MCI).

2. History

• Petersen R.C. (1999) — clinical conceptualization of MCI.
• DSM-5 (2013) — Major (dementia) and Mild Neurocognitive Disorders categories.
• AAN (2018) — Practice Guideline for MCI (Petersen).

3. Epidemiology

• Prevalence 10–20% in those aged 65+.
• Annual 10–15% of MCI transition to Alzheimer dementia.
• Risk factors: age, ApoE4, cardiovascular.

4. Aetiology and pathogenesis

• Alzheimer's prodromal (amnestic MCI);
• Vascular
• Lewy bodies prodromal;
• Frontotemporal;
• Medical (depression, thyroid, B12, medication effects).

5. Clinical features

• The patient or a close person complains of cognitive decline.
• Mild deficit on standardized tests (typically -1 to -2 SD).
• Daily functioning is preserved (minimal compensation in complex activities).
• Subtypes: amnestic (memory dominant — high Alzheimer's risk), non-amnestic (executive or other domain).

6. Diagnosis

6.1 Unified diagnostic criteria

A. Mild decline in one or more cognitive domains (noted by patient, informant, or clinician, and standardized neuropsychological testing).

B. Daily functioning is preserved.

C. Not better explained by delirium

D. Not better explained by another mental disorder (MDD).

6.2 Source-specific clarifications

• DSM-5-TR — separation of Major and Mild.
• AAN 2018 — etiological investigation (Alzheimer, vascular) and biomarkers in developmental stage.

6.3 Diagnostic algorithm

1. Clinical interview + informant.
2. MoCA (Montreal Cognitive Assessment), MMSE.
3. Neuropsychological testing.
4. Laboratory — B12, folate, TSH, liver, kidney, glucose, HIV/syphilis.
5. Brain MRI — vascular, atrophy, other pathology.
6. Biomarkers (if clinical suspicion) — CSF amyloid-β/tau, PET imaging (Alzheimer's prodrome).
7. Depression screening (GDS, PHQ-9).

6.4 Differential diagnosis

7. Examination and assessment

• MoCA (≤ 25 pathological) — the validated screen for MCI; MMSE has no established MCI cut-off and is insensitive to mild impairment.
• Neuropsychological battery (memory, executive, language, visuospatial).
• Laboratory panel.
• MRI (routine), biomarkers (selective).

8. Treatment

1. Etiological treatment — modifiable factors (cardiovascular risk, B12, thyroid, depression, medication).
2. Lifestyle — physical activity (aerobic), Mediterranean diet, cognitive stimulation, social connections (FINGER trial Lancet 2015 – multimodal approach effective).
3. Pharmacotherapy — no specific approval for MCI. Donepezil and other AChEIs — limited evidence base; not routinely recommended.
4. Lecanemab, Donanemab — new anti-amyloid antibodies; FDA approval (lecanemab 2023, donanemab 2024) for Alzheimer prodrome and mild dementia; clinical effect modest, infusion reactions and ARIA (Amyloid-Related Imaging Abnormalities) risk.
5. Comorbid depression, anxiety treatment (SSRIs).
6. Monitoring risk of transition to dementia.

Source-specific specifications

• AAN 2018 — modifiable factors and lifestyle.
• FINGER trial (Ngandu Lancet 2015) — multimodal intervention.
• Lecanemab — CLARITY-AD (van Dyck NEJM 2023); donanemab — TRAILBLAZER-ALZ 2 (Sims JAMA 2023).

Treatment methods

1. Montreal Cognitive Assessment (MoCA) — Nasreddine Z.S — 30 items; MCI screening (cut-off 26).
2. FINGER Multimodal Intervention (FINGER — Finnish Geriatric Intervention Study) — Diet + exercise + cognitive training + vascular risk management.
3. Lecanemab, Donanemab — Anti-amyloid antibodies; FDA approval; ARIA monitoring (MRI).

9. Prognosis

• Stable 30%, transition to dementia 10–15%/year, reversion to normal cognition 15–20%.
• Amnestic MCI as Alzheimer's prodrome — high conversion rate.

10. Myths and misconceptions

Myth 1: “MCI inevitably turns into dementia”

Evidence: annual rate 10–15%; some remain stable or improve.

Myth 2: “Vitamin B and ginkgo cure MCI”

Evidence: B vitamins only in deficiency; ginkgo Cochrane (Birks 2009) — weak evidence of effect.

Myth 3: “AChEI is the standard treatment for MCI”

Evidence: AAN 2018 — evidence base insufficient; not routinely recommended.

Myth 4: “Lecanemab cures MCI/Alzheimer's”

Evidence: Reduces clinical decline rate by ~25%; ARIA and infusion reactions; not “cure.”

Myth 5: “Cognitive decline is inevitable with age”

Evidence: Cardiovascular risk, physical activity, social connections are modifiable factors.

11. Sources

1. WHO. ICD-11. 6D71 Mild neurocognitive disorder. 2024.
2. APA. DSM-5-TR. 2022.
3. Petersen R.C. et al. Practice guideline update summary: Mild cognitive impairment. Neurology 2018;90(3):126–135.
4. Ngandu T. et al. A 2-year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring (FINGER): a randomised controlled trial. Lancet 2015;385(9984):2255–2263.
5. van Dyck C.H. et al. Lecanemab in Early Alzheimer's Disease. NEJM 2023;388(1):9–21.
6. Nasreddine Z.S., Phillips N.A., Bédirian V. et al. The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc 2005;53(4):695–699.
7. Birks J., Grimley Evans J. Ginkgo biloba for cognitive impairment and dementia. Cochrane Database Syst Rev 2009;(1):CD003120.