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Articles by A. M. Jacobson
Total Records ( 2 ) for A. M. Jacobson
  I. K Lyoo , S. J Yoon , G Musen , D. C Simonson , K Weinger , N Bolo , C. M Ryan , J. E Kim , P. F Renshaw and A. M. Jacobson

Context  Neural substrates for low cognitive performance and depression, common long-term central nervous system–related changes in patients with type 1 diabetes mellitus, have not yet been studied.

Objective  To investigate whether prefrontal glutamate levels are higher in patients with type 1 diabetes and whether an elevation is related to lower cognitive performance and depression.

Design  Cross-sectional study.

Setting  General clinical research center.

Participants  One hundred twenty-three patients with adult type 1 diabetes with varying degrees of lifetime glycemic control and 38 healthy participants.

Main Outcome Measures  With the use of proton magnetic resonance spectroscopy, prefrontal glutamate–glutamine–-aminobutyric acid (Glx) levels were compared between patients and control subjects. Relationships between prefrontal Glx levels and cognitive function and between Glx levels and mild depressive symptoms were assessed in patients with type 1 diabetes.

Results  Prefrontal Glx concentrations were 9.0% (0.742 mmol/L; P = .005) higher in adult patients with type 1 diabetes than in healthy control subjects. There were positive linear trends for the effects of lifetime glycemic control on prefrontal Glx levels (P for trend = .002). Cognitive performances in memory, executive function, and psychomotor speed were lower in patients (P = .003, .01, and <.001, respectively) than in control subjects. Higher prefrontal Glx concentrations in patients were associated with lower performance in assessment of global cognitive function (0.11 change in z score per 1-mmol/L increase in Glx) as well as with mild depression.

Conclusions  The high prefrontal glutamate levels documented in this study may play an important role in the genesis of the low cognitive performance and mild depression frequently observed in patients with type 1 diabetes. Therapeutic options that alter glutamatergic neurotransmission may be of benefit in treating central nervous system–related changes in patients with adult type 1 diabetes.

  A. M. Jacobson , A. D. Paterson , C. M. Ryan , P. A. Cleary , B. H. Waberski , K. Weinger , G. Musen , W. Dahms , M. Bayless , N. Silvers , J. Harth , A. P. Boright and The DCCT/EDIC Research Group
  Aims  Specific polymorphisms of the apolipoprotein E (APOE) and angiotensin-converting enzyme (ACE) genes appear to increase risk for Alzheimer's disease and cognitive dysfunction in the general population, yet little research has examined whether genetic factors influence risk of cognitive dysfunction in patients with Type 1 diabetes. The long-term follow-up of the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) population provides an opportunity to examine if specific genetic variations in APOE and ACE alter risk for cognitive decline.
Methods  Neurocognitive function in Type 1 diabetic subjects from the DCCT/EDIC study was assessed at DCCT entry and re-assessed approximately 18 years later, using a comprehensive cognitive test battery. Glycated haemoglobin (HbA 1c ) and the frequency of severe hypoglycaemic events leading to coma or seizures were measured over the 18-year follow-up. We determined whether the APO ε4 and ACE intron 16 indel genotypes were associated with baseline cognitive function and with change over time, and whether they conferred added risk in those subjects experiencing severe hypoglycaemic events or greater glycaemic exposure.
Results  None of the APOE or ACE polymorphisms were associated with either baseline cognitive performance or change in cognition over the 18-year follow-up. Moreover, none of the genotype variations altered the risk of cognitive dysfunction in those subjects with severe hypoglycaemic episodes or high HbA 1c .
  In this sample of young and middle-aged adults with Type 1 diabetes, APO ε4 and ACE D alleles do not appear to increase risk of cognitive dysfunction.
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