The edition · Neurology
Depression in cerebral amyloid angiopathy is fifteen times more likely, and it tracks the cortex
A two-site study finds depressive symptoms in CAA are common, correlate with siderosis and cortical thinning, and mediate part of the cognitive deficit. Plus what plasma p-tau217 timing really predicts, and a marker of reperfusion injury after thrombectomy.
The edition in brief
The neurology desk today is about the things sitting alongside the diagnosis. In 85 people with probable cerebral amyloid angiopathy and 83 controls, CAA carried an odds ratio of 15.71 (95% CI 4.26-80.05) for possible depression on the GDS-15, with scores 2.71 times higher than controls. Depressive symptoms mediated 11% of the effect of CAA on episodic memory and 9% on executive function, but nothing on processing speed. Within the CAA group, higher depression scores tracked lower mean cortical thickness and the presence of cortical superficial siderosis - suggesting some of the mood disturbance is cortical damage rather than reaction to diagnosis. A modelling study across 2369 Mayo Clinic Study of Aging and 1591 ADNI participants asked how well the timing of plasma p-tau217 and PET biomarkers predicts the timing of cognitive decline. In the population-based sample, plasma p-tau217 accounted for 16% of the variability in the timing of verbal learning decline; in the Alzheimer's-enriched cohort it accounted for 64%. That gap is the finding, and it is a warning about generalising biomarker performance from enriched cohorts to clinic populations. In 229 thrombectomy patients, a hyperintense acute reperfusion marker on post-contrast FLAIR was present in 48.9% and was independently associated with early neurological deterioration (adjusted odds ratio 3.45, 95% CI 1.33-8.95) and infarct growth (2.46, 95% CI 1.22-4.95), though not with three-month function. A joint internal medicine and retina society position statement sets out a shared pathway for anterior ischaemic optic neuropathy.
Depressive symptoms in cerebral amyloid angiopathy track cortical damage, not just distress
Screen for depression in every patient with cerebral amyloid angiopathy, and retest cognition after treating it before calling the impairment fixed.
Plasma p-tau217 explained 16% of cognitive timing in the community and 64% in a trial cohort
Treat plasma p-tau217 as a reasonable progression marker but expect far weaker performance in an unselected clinic than the published cohort figures suggest.
A reperfusion marker that predicts early deterioration but not three-month outcome
If the reperfusion marker is present after thrombectomy, increase observation frequency for 48 hours - but do not use it to predict three-month recovery.
Sudden painless monocular vision loss over 50 is a same-day question, not a clinic referral
In sudden painless monocular vision loss over 50, answer the arteritic question the same day and start steroids on suspicion rather than waiting for biopsy.
A joint pathway for ischaemic optic neuropathy, and where the evidence runs out
Adopt a written local pathway naming who does the vascular workup and follow-up after ischaemic optic neuropathy, rather than assuming the eye clinic has it.
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