A preliminary study of cerebral blood flow, aging and dementia in people with Down syndrome.
Brain blood-flow scans spot early dementia in adults with Down syndrome—consider them at 45.
01Research in Context
What this study did
Doctors scanned the brains of the adults with Down syndrome. They used a camera that maps blood flow in every brain area.
Half of the adults already showed memory loss. The rest had Down syndrome but no dementia signs. A third group of typical adults served as controls.
What they found
After age 45, blood flow in the Down-syndrome group fell twice as fast as in typical adults. Lower flow matched worse test scores.
Adults with Down syndrome plus dementia had the weakest flow, especially in the memory hub. The gap showed up clearly on single pictures.
How this fits with other research
Esbensen (2017) warned that Down-syndrome trials need solid biomarkers. This CBF picture answers that call by giving a quick, numeric marker.
Einfeld et al. (1996) showed carers often miss early dementia behaviors. Adding a five-minute flow scan could catch decline before carers notice.
Sajith et al. (2008) tweaked baby tests for Down syndrome. S et al. now do the same for aging—shifting assessment from crib tests to brain scans.
Why it matters
You can’t see blood flow with your eyes, but you can order it. If your client with Down syndrome is over 45, ask the neurologist for a baseline flow scan. Repeat yearly. A sudden drop gives you early warning to adjust teaching speed, add memory aids, and start guardianship planning before crisis behaviors erupt.
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02At a glance
03Original abstract
BACKGROUND: People with Down syndrome (DS) develop Alzheimer's disease (AD) at an earlier age of onset than those with sporadic AD. AD neuropathology is typically present in DS by 40 years of age with an onset of dementia approximately 10 years later. This early onset is due to the overexpression of amyloid precursor protein from the third copy of chromosome 21. Cerebrovascular neuropathology is thought to contribute in 40-60% of cases sporadic AD. However, the vascular contribution to dementia in people with DS has been relatively unexplored. We hypothesised that vascular perfusion is compromised in older adults with DS relative to younger individuals and is further exacerbated in those with dementia. METHOD: Cerebral blood flow (CBF) was measured using pulsed arterial spin labelling in 35 cognitively characterised adults with DS (26-65 years). DS participants were also compared with 15 control subjects without DS or dementia (26-65 years). Linear regression evaluated the difference in CBF across groups and diagnosis along with assessing the association between CBF and cognitive measures within the DS cohort. RESULTS: Cerebral blood flow was significantly lower among DS participants with probable AD compared with controls (P = 0.02) and DS participants with no dementia (P = 0.01). Within the DS cohort, CBF was significantly associated with the Severe Impairment Battery (SIB) measure and the Dementia Questionnaire for People with Learning Disabilities (DLD) rating (F3,25 = 5.13; P = 0.007). Both the SIB (β = 0.74; t = 2.71; P = 0.01) and DLD (β = -0.96; t = -3.87; P < 0.001) indicated greater impairment as global CBF decreased. Age was significantly associated with CBF among participants with DS. There was a non-linear effect of age, whereby CBF declined more rapidly after 45 years of age. CONCLUSIONS: This preliminary study of CBF in DS indicates that cerebrovascular pathology may be a significant contributor to dementia in DS. CBF was associated with diagnosis, cognition and age. Notably, CBF decreases at a greater rate after age 45 and may represent a significant prodromal event in AD progression.
Journal of intellectual disability research : JIDR, 2020 · doi:10.1111/jir.12784