Chiodini and colleagues (1) reported that increased levels of cortisol secretion are related to diabetes complications but did not evaluate central nervous system complications. It has been increasingly recognized that diabetes is related to several neurological and psychiatric disorders. Mild cognitive impairment, Alzheimer's disease, and depression have been associated with diabetes, and these are also related to abnormal cortisol levels. The discovery of how hypercortisolism is related to diabetes complications could help us understand these associations.

It has been known that Cushing's syndrome (a hypercortisolemic condition) is related to neuropsychological impairment, probably mediated by cortisol deleterious effects in the brain (2). Moreover, treatment of depression in diabetic patients has led to improvement in glycemic and diabetes complications (3). Glucocorticoid-related memory impairment has been linked to glucocorticoid receptors in the hippocampus (4), and it is said that cortisol predicts cognitive functions (5). Glucocorticoids have been shown to increase the pathogenic features of Alzheimer's disease (6), and in addition, rosiglitazone, an insulin sensitizer, has shown to reverse memory deficits in a transgenic model of Alzheimer's disease by reducing glucocorticoid actions (7). Earlier, Sandeep et al. (8) showed that blocking 11β-hydroxisteroid dehydrogenase, which normally regenerates cortisone to cortisol, improved cognitive performance in a diabetic group.

In light of the finding made by Chiodini et al. (1), cortisol should become a focal point in researching diabetes complications.

J.M.P.-O. is partially supported by PRIORI-UADY (FMED 06-004).

1.
Chiodini I, Adda G, Scillitani A, Coletti F, Morelli V, Di Lembo S, Epaminonda P, Masserini B, Beck-Peccoz P, Orsi E, Ambrosi B, Arosio M: Cortisol secretion in patients with type 2 diabetes: relationship with chronic complications.
Diabetes Care
 
30
:
83
–88,
2007
2.
Forget H, Lacroix A, Somma M, Cohen H: Cognitive decline in patients with Cushing's syndrome.
J Int Neuropsychol Soc
 
6
:
20
–29,
2000
3.
Simon GE, Katon WJ, Lin EH, Rutter C, Manning WG, Von Korff M, Ciechanowski P, Ludman EJ, Young BA: Cost-effectiveness of systematic depression treatment among people with diabetes mellitus.
Arch Gen Psychiatry
 
64
:
65
–72,
2007
4.
Roozendaal B, Griffith QK, Buranday J, de Quervain DJ, McGaugh JL: The hippocampus mediates glucocorticoid-induced impairment of spatial memory retrieval: dependence on the basolateral amygdale.
Proc Natl Acad Sci U S A
 
100
:
1328
–1333,
2003
5.
Egeland J, Lund A, Landro NI, Rund BR, Sundet K, Asbjornsen A, Mjellem N, Roness A, Stordal KI: Cortisol predicts executive and memory function in depression, symptom level predicts psychomotor speed.
Acta Psychiatr Scand
 
112
:
434
–441,
2005
6.
Green KN, Billings LM, Roozendaal B, McGaugh JL, LaFerla FM: Glucocorticoids increase amyloid-β and tau pathology in a mouse model of Alzheimer's disease.
J Neurosci
 
26
:
9047
–9056,
2006
7.
Pedersen WA, McMillan PJ, Kulstad JJ, Leverenz JB, Craft S, Haynatzki GR: Rosiglitazone attenuates learning and memory deficits in Tg2576 Alzheimer disease.
Exp Neurol
 
199
:
265
–273,
2006
8.
Sandeep TC, Yau JL, MacLullich AM, Noble J, Deary IJ, Walker BR, Seckl JR: 11 β-hidroxysteroid dehydrogenase inhibition improves cognitive function in healthy elderly men and type 2 diabetics.
Proc Natl Acad Sci U S A
 
101
:
6734
–6739,
2004
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