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P2‐371: Elevated diastolic blood pressure predicts poorer verbal memory in MCI adults with prediabetes
Author(s) -
Skinner Jeannine,
Cholerton Brenna,
Watson G. Stennis,
Callaghan Maureen,
Hanson Angela,
Craft Suzanne,
Baker Laura
Publication year - 2012
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2012.05.1081
Subject(s) - prediabetes , blood pressure , medicine , glycated hemoglobin , diabetes mellitus , cognitive decline , type 2 diabetes , dementia , risk factor , cardiology , disease , endocrinology
Background:Although mild cognitive impairment is considered a high risk factor for dementia, there is no pharmacological treatment available for this condition. Some nonpharmacological intervention studies have suggested a benefit of memory functioning and activities of daily living in MCI patients receiving a cognitive and/or physical training regimen. There is growing evidence that plasma brain-derived neurotrophic factor (BDNF) plays an important role in the pathogenesis of AD. Methods: Randomized, controlled study using a 12 week combined cognitive-motor intervention in 38 patients with amnestic MCI and 21 healthy controls at the age of 55 to 75 years. Out of the subjects with aMCI 19 were included in the training, 19 were regarded as waiting list. Neuropsychological assessment, consisting of visual and verbal episodic memory tests as well as verbal short term and working memory tests, MRI for hippocampal volume measurements and BDNF plasma analysis were drawn at baseline and at the end of the study. Moreover, short-term BDNF changes were measured at four intervention days. Results: Long term assessment showed an improvement in episodic memory in aMCI subjects (AVLT sum: T 1⁄4 -5.0, df 1⁄4 16, P < .001) and healthy controls (AVLT sum: T 1⁄4 -2.3, df 1⁄4 18, P 1⁄4 .033). Memory improvement was associated in both groups with hippocampal growth (aMCI: AVLT sum r 1⁄4 .348, P 1⁄4 .05; healthy controls: AVLT sum: r 1⁄4 .550, P 1⁄4 .03) and in healthy controls with BDNF increase (AVLT sum: r 1⁄4 .473, P 1⁄4 .04), while in aMCI a change of BDNF during the intervention was not observed. BDNF increased in healthy controls during long term follow-up (T1⁄4 -2.1, df1⁄4 17, P1⁄4 .05) as well as in short term effect before and after a single training bout. Contrasting in aMCI short term changes demonstrated an increasing drop of BDNF towards the end of the study. Conclusions: These findings support the utility of a cognitive intervention in aMCI that is comparable to that in healthy controls. However it yields evidence that underlying mechanisms are different pointing to an impaired BDNF modulation in aMCI.