The role of metabolic derangements and glucocorticoid excess in the aetiology of cognitive impairment in type 2 diabetes. Implications for future therapeutic strategies

Diabetes, Obesity and Metabolism

Volumn 11, Issue 5, 2009, Pages 407-414

  Strachan, Mark W J ^a   Reynolds, Rebecca M ^b   Frier, Brian M ^c   Mitchell, Rory J ^d   Price, Jacqueline F ^d  

^a WESTERN GENERAL HOSPITAL   (United Kingdom)

^b UNIVERSITY OF EDINBURGH   (United Kingdom)

^c ROYAL INFIRMARY OF EDINBURGH   (United Kingdom)

^d UNIVERSITY OF EDINBURGH   (United Kingdom)

Author keywords

Cognition; Cortisol; Dementia; Hyperinsulinaemia; Type 2 diabetes

Indexed keywords

2,4 THIAZOLIDINEDIONE DERIVATIVE; CARBENOXOLONE; GLIBENCLAMIDE; GLUCOCORTICOID; INSULIN; METFORMIN; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA AGONIST; PLACEBO; REPAGLINIDE; ROSIGLITAZONE;

ALZHEIMER DISEASE; CLINICAL TRIAL; COGNITIVE DEFECT; DEMENTIA; DISEASE ASSOCIATION; GENETIC PREDISPOSITION; GLYCEMIC CONTROL; HIPPOCAMPUS; HUMAN; HYDROCORTISONE BLOOD LEVEL; HYPERGLYCEMIA; HYPERINSULINEMIA; HYPOTHALAMUS HYPOPHYSIS ADRENAL SYSTEM; INSULIN RESISTANCE; INSULIN SENSITIVITY; METABOLIC DISORDER; MILD COGNITIVE IMPAIRMENT; NERVE DEGENERATION; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; REVIEW; VERBAL MEMORY; WORKING MEMORY;

EID: 65449167566     PISSN: 14628902     EISSN: 14631326     Source Type: Journal    
DOI: 10.1111/j.1463-1326.2008.00963.x     Document Type: Review

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