Association between total-Tau and brain atrophy one year after first-ever stroke.

BACKGROUND: Although the most serious consequence of neuronal ischemia is acute neuronal death, mounting evidence suggests similarities between stroke and neurodegenerative disease. Brain atrophy visualized on structural MRI and pathological cerebrospinal fluid (CSF) concentrations of microtubule-associated protein tau (T-tau) and phosphorylated microtubule-associated protein tau indicate neurofibrillary degeneration. We aimed to explore the association between CSF T-tau and brain atrophy 1 year post-stroke. METHODS: We included 210 patients with first-ever ischemic stroke or transitory ischemic attack without pre-existing cognitive impairment. After 12 months, subjects underwent MRI, and CSF biomarkers were assessed. Using SIENAX (part of FSL), ventricular CSF volume and total brain volume were estimated and normalized for subject head size. The association between T-tau as explanatory variable and ventricular and total brain volume as outcome variables were studied using linear regression. RESULTS: One hundred eighty-two patients completed the follow-up. Forty-four had a lumbar puncture. Of these, 31 had their MRI with identical scan parameters. Mean age was 70.2 years (SD 11.7). Ventricular volume on MRI was significantly associated with age, but not with gender. In the multiple regression model, there was a significant association between T-tau and both ventricular (beta 0.44, 95% CI 376.3, 394.9, p = 0.021) and global brain volume (beta -0.50, 95% CI -565.9, -78.3, p = 0.011). There was no significant association between CSF T-tau 1 year post-stroke and baseline volumes. CONCLUSION: T-tau measured 1 year post-stroke is associated with measures of brain atrophy. The findings indicate that acute stroke may enhance or trigger tau-linked neurodegeneration with loss of neurons. TRIAL REGISTRATION: Clinicaltrials.gov NCT00506818 , July 23, 2007. Inclusion from February 2007, randomization and intervention from May 2007 and trial registration in July 2007.

Blood pressure control to prevent decline in cognition after stroke.

BACKGROUND: Treatment of hypertension post-stroke preserves cognition through prevention of recurrent stroke, but it is not clear whether it prevents cognitive decline through other mechanisms. We aimed to describe changes in blood pressure from baseline to 1 year post-stroke and to evaluate the association between achieved blood pressure targets and cognitive function, mild cognitive impairment (MCI), and dementia. METHODS: We included patients with first-ever stroke, and defined achieved blood pressure goals as systolic blood pressure (SBP) in the categories ≤125 mmHg, ≤140 mmHg, and ≤160 mmHg, SBP reduction of ≥10 mmHg, and diastolic blood pressure (DBP) reduction of ≥5 mmHg. The main outcome variables were cognitive assessments 1 year post stroke. Secondary outcomes were diagnoses of MCI or dementia. RESULTS: Forty-one of 166 patients (25%) reached SBP ≤125 mmHg after 1 year, 92/166 (55%) reached SBP ≤140 mmHg, and 150/166 (90%) reached SBP ≤160 mmHg. SBP was reduced by ≥10 mmHg in 44/150 (29%) and DBP by ≥5 mmHg in 57/150 (38%). We did not find any statistically significant associations between cognitive test performances and different blood pressure goals (P=0.070-1.0). Nor was there any significant association between achieved goal blood pressure or blood pressure reduction after 1 year and the diagnoses of MCI or dementia (P=0.32-0.56). CONCLUSION: Treatment of hypertension is important for primary and secondary prevention of stroke. Showing a potential beneficial effect of blood pressure control on cognitive function, however, probably needs longer follow-up.

Multifactorial vascular risk factor intervention to prevent cognitive impairment after stroke and TIA: a 12-month randomized controlled trial.

OBJECTIVES: Vascular risk factor control may not only prevent stroke but also reduce the risk of dementia. We investigated whether a multifactorial intervention program reduces the incidence of cognitive symptoms one-year after stroke and transient ischemic attack in first ever stroke patients without cognitive decline prior to the stroke. MATERIALS AND METHODS: Patients suffering their first ever stroke were included in this randomized, evaluator-blinded, controlled trial with two parallel groups. Baseline examination included extensive assessment of exposure to vascular risk factors and cognitive assessments regarding memory, attention, and executive function. After discharge, patients were allocated to either intensive vascular risk factor intervention or care as usual. The primary end points were changes in trailmaking test A and 10-word test from baseline to 12 months follow-up. RESULTS: One hundred ninety-five patients were randomized. The difference between groups in trail-making test A, adjusted for baseline measurements, was 3·8 s (95% confidence interval: -4·2 to 11·9; P=0·35) in favor of the intervention group. The difference between groups in the 10-word recall test was 1·1 words (95% confidence interval: -0·5 to 2·7; P=0·17) in favor of the intervention group. We did not observe any differences in the secondary outcomes of incident dementia or mild cognitive impairment. CONCLUSIONS: We could not demonstrate cognitive effects of an intensive risk factor intervention at one-year poststroke. Longer follow-up and a more heterogeneous study sample might have lead to larger effects. More effective methods for managing the risk of further cognitive decline after stroke are needed.