Down syndrome and mental health (MEQ)

(i) Priority differentials. Major depression; Alzheimer-type dementia (DS-associated); mixed depression and emerging dementia; hypothyroidism; obstructive sleep apnoea; sensory impairment (hearing/vision); delirium/infection; medication effects; pain/constipation; grief or environmental change; abuse/neglect. Do not collapse to “only Alzheimer” on first presentation.[1][3][7]

(ii) Assessment. Developmental baseline from prior reports and carer timeline of skill loss. ID-adapted MSE with collateral. Risk (self-neglect, fluid/food intake, exploitation). Investigations: TSH/free T4, B12/folate, FBC, U&E/glucose, infection screen if indicated, medication review, hearing and vision, sleep/OSA pathway given snoring. Capacity is decision-specific with supported decision-making under local law.[1][7]

(iii) Mechanism. Trisomy 21 includes APP gene triplication → lifelong amyloid overproduction → early Alzheimer neuropathology and high clinical dementia risk; biomarker cascades map an Alzheimer continuum in adults with DS.[2][4]

(iv) Tools. DSQIID as observer-rated screen for dementia in ID; modified CAMDEX informant interview / CAMDEX-DS tradition as structured support for diagnosis. Serial adaptive function comparison is essential; neuropathology alone is not clinical dementia.[5][6][2]

(v) Management branches. If depression primary after medical work-up: adapted psychological support plus SSRI start-low go-slow (e.g. sertraline oral 25 mg daily initially, slow titration, monitor adverse effects and response), carer education, rebuild day structure; reassess cognition after mood recovers.[7] If progressive Alzheimer dementia confirmed: environmental simplification, PBS for BPSD, treat sensory/medical drivers, carer respite, individualised specialist consideration of dementia drugs, advance care planning and dementia-capable services; avoid therapeutic nihilism and avoid antipsychotic-first for environmental behaviour.[2][3][8]