REVIEW PAPER
COGNITIVE FUNCTIONS DISORDERS IN DIABETES
 
More details
Hide details
1
Z Kliniki Endokrynologii UM w Lublinie
2
Z Katedry i Zakładu Medycyny Rodzinnej UM w Lublinie
3
Z Oddziału Nefrologii, Endokrynologii, Chorób Metabolicznych i Chorób Wewnętrznych ze stacją dializ SPSW im Papieża Jana Pawła II w Zamościu
 
Med Og. 2009;15(2):191–201
 
KEYWORDS
ABSTRACT
The precondition for an understanding of the treatment of diabetes, specification of personal health goals, as well as motivation and adequate attitude towards treatment are undoubtedly non-disrupted cognitive functions. The weakening of these functions is a factor which, to a considerable degree, hinders treatment and co-operation with a patient. It has been confirmed that in the course of diabetes there occurs impairment of the cognitive functions, and the process seems to be closely connected with the duration of the disease, degree of metabolic control and presence of chronic complications. In diabetics, a decreased psychomotor pace is observed, a deteriorated concentration selectivity and capability for analysing complex information, as well as worsening of memory. Among the causes of the occurrence of cognitive functions disorders, diabetic encephalopathy is most frequently mentioned, caused by chronic hyperglycemia lasting for years, and transitory, repeated states of hypoglycemia – a direct effect of insulin, presence of chronic complications, and even more frequent occurrence of Alzheinmer’s disease among diabetic patients. Disorders of carbohydrates metabolism present in diabetes exert an important effect on neurotransmission in the CNS, which is not without influence on the patient’s cognitive functions. In order to increase the effectiveness of care of diabetic patients, the introduction of simple screening tests evaluating cognitive functions seems justifiable. The distinguishing of a group of people with cognitive functions disorders would enable covering them with proper care, and allow the adjustment of doctor’s recommendations to the cognitive capabilities of patients.
 
REFERENCES (46)
1.
Amiel SA: Glucose counterregulation in health and disease: current concepts in hypoglycaemia recognition and response. Q. J. Med. 1991, 293, 707-727.
 
2.
Amiel SA, Archibald HR, Chusney G, Williams AJ, Gale EA: Ketone infusion lowers hormonal responses to hypoglycaemia: evidence for acute cerebral utilisation of a non glucose fuel. Clin. Sci. 1991, 81, 189-194.
 
3.
Auer RN: Hypoglycemic brain damage. Metab Brain Dis. 2004, 19 (3-4), 169-175.
 
4.
Benedict C, Hallschmid M, Hatke A, Schultes B, Fehm HL, Born J i wsp.: Intranasal insulin improves memory in humans. Psychoneuroendocrinology. 2004, 29(10), 1326-1334.
 
5.
Bjorgaas M, Gimse R, Vik T, Sand T.:Cognitive function in type 1 diabetic children with and without episodes of severe hypoglycaemia.Acta Paediatr. 1997, 86 (2), 148-153.
 
6.
Bushe C, Holt R: Prevalence of diabetes and impaired glucose tolerance in patients with schizophrenia. Br J Psychiatry 2004, 47, S67-S71.
 
7.
Chen CC, Yang JC: Effects of short and long-lasting diabetes mellitus on mouse brain monoamines. Brain Res. 1991, 552 (1), 175-179.
 
8.
Chmiel-Perzyńska I, Szyprowska E, Perzyński A, Masiak M: Współwystępowanie schizofrenii i zaburzeń gospodarki węglowodanowej. Badania nad Schizofrenią. 2005, VI, 6, 73-80.
 
9.
Coscelli C, Calabrese G, Fedele D i wsp.: Use of premixed insulin among the elderly.Reduction of error in patient preparation of mixtures. Diabetes Care. 1992, 15, 1628-1630.
 
10.
Craft S, Watson GS.:Insulin and neurodegenerative disease: shared and specific mechanisms. Lancet Neurol. 2004, 3 (3), 169-178.
 
11.
Davis EA, Soong SA, Byrne GC, Jones TW: Acute hyperglycaemia impairs cognitive function in children with IDDM. J Pediatr Endocrinol Metab. 1996, 9 (4), 455-461.
 
12.
Derkacz M, Marczewski K, Maciejewski M: Przydatność badania funkcji poznawczych na przykładzie testu rysowania zegara w ocenie stanu klinicznego chorych na cukrzycę Fam. Med. Prim. Care Rev. 2007, 9 (3), 411-414.
 
13.
Derkacz M, Sawicka A, Marczewski K: Łagodne zaburzenia funkcji poznawczych u chorych na cukrzycę — obserwacje ośrodka terenowego. Diabetol. Dośw. Klin. 2005, 5, 273–278.
 
14.
Fishel MA, Watson GS, Montine T: Hyperinsulinemia Provokes Synchronous Increases in Central Inflammation and β-Amyloid in Normal Adults. Arch Neurol. 2005, 62, 1539-1544.
 
15.
Flykanaka-Gantenbein C: Hypoglycemia in childhood: long-term effects. Pediatr Endocrinol Rev. 2004, 1 (3), 530-536.
 
16.
Freychet P: Insulin receptors and insulin actions in the nervous system. : Diabetes Metab Res Rev. 2000; 16 (6), 390-392.
 
17.
Fujioka M, Okuchi K, Hiramatsu KI, Skaki T, Sakaguchi S, Ishii Y: Specific changes in human brain after hypoglycemic injury. Stroke 1997, 28, 584-587.
 
18.
Gasparini L, Netzer WJ, Greengard P, Xu H: Does insulin dysfunction play a role in Alzheimer's disease?Trends Pharmacol Sci. 2002, 23 (6), 288-293.
 
19.
Gerozissis K: Brain insulin: regulation, mechanisms of action and functions. Cell Mol Neurobiol. 2003, 23 (1), 1-25.
 
20.
Gerozissis K: Brain insulin and feeding: a bi-directional communication. Eur J Pharmacol. 2004, 490 (1-3), 59-70.
 
21.
Gerozissis K, Rouch C, Lemierre S, Nicolaidis S: A potential role of central insulin in learning and memory related to feeding Cellular and Molecular Neurobiology. 2001, 21 (4), 389-401.
 
22.
Gotoh M, Li C, Yatoh M, Okabayashi N, Habu S, Hirooka Y: Hypothalamic monoamine metabolism is different between the diabetic GK (Goto-Kakizaki) rats and streptozotocin-induced diabetic rats. Brain Res. 2006, 1073-1074, 497-501.
 
23.
Hili JM, Leśniak MA, Pert CB, Roth J: Autoradiographic localization of insulin receptors in rat brain: prominences in olfactory and limbic areas. Diabetologica. 1986, 17, 1128-1138.
 
24.
Hoyer S: Is sporadic Alzheimer disease the brain type of non-insulin dependent diabetes mellitus? A challenging hypothesis.J Neural Transm. 1998, 105 (4-5), 415-422.
 
25.
Iino K, Yoshinari M, Yoshizumi H, Ichikawa K, Iwase M, Fujishima M: Normal pressure hydrocephalus in diabetic patients with recurrent episodes of hypoglycemic coma. Diabetes Res Clin Pract. 2000, 47 (2), 105-110.
 
26.
Janson J, Laedtke T, Parisi JE, O'Brien P, Petersen RC, Butler PC.:Increased risk of type 2 diabetes in Alzheimer disease.Diabetes. 2004, 53 (2), 474-481.
 
27.
Kalimo H, Olsson Y: Effects of severe hypoglycemia on the human brain. Neuropathological case reports. Acta Neurol Scand. 1980, 62 (6), 345-356.
 
28.
Martin P, Massol J, Pichat P, Puech AJ: Decreased central GABA B receptor binding sites in diabetic rats. Neuropsychobiology. 1988, 19 (3), 146-148.
 
29.
McCall AL: Cerebral glucose metabolism in diabetes mellitus. Eur J Pharmacol. 2004, 490 (1-3), 147-158.
 
30.
Meikle A, Riby LM, Stollery B: The impact of glucose ingestion and gluco-regulatory control on cognitive performance: a comparison of younger and middle aged adults. Hum Psychopharmacol. 2004, 19 (8), 523-535.
 
31.
Mooradian AD: Blood-brain barrier choline transport is reduced in diabetic rats. Diabetes, 1987, 36 (10), 1094-1097.
 
32.
Moosavi M, Naghdi N, Maghsoudi N, Zahedi Asl S: The effect of intrahippocampal insulin microinjection on spatial learning and memory. Horm Behav. 2006, 50 (5), 748-752.
 
33.
Padayatti PS, Paulose CS: Alpha2 adrenergic and high affinity serotonergic receptor changes in the brain stem of streptozotocin-induced diabetic rats. Life Sci. 1999, 65 (4), 403-414.
 
34.
Rovet JE, Ehrlich RM., Hoppe M.: Intellectual deficits associated with early onset of insulin-dependent diabetes mellitus in children. Diabetes Care 1987, 10, 510-515.
 
35.
Ryan CM, Geckle M: Why is learning and memory dysfunction in Type 2 diabetes limited to older adults? Diabetes Metab Res Rev. 2000, 16 (5), 308-315.
 
36.
Sandrini M, Vitale G, Vergoni AV, Ottani A, Bertolini A: Streptozotocin-induced diabetes provokes changes in serotonin concentration and on 5-HT1A and 5-HT2 receptors in the rat brain. Life Sci. 1997, 60 (16), 1393-1397.
 
37.
Sima AA, Kamiya H, Li ZG: Insulin, C-peptide, hyperglycemia, and central nervous system complications in diabetes. Eur J Pharmacol. 2004, 490 (1-3), 187-197.
 
38.
Sinclair AJ, Girling AJ, Bayer AJ: Cognitive dysfunction in older subjects with diabetes mellitus: impact on diabetes self-management and use of care services. Diabetes Res Clin Prac.2000, 50, 203-212.
 
39.
Suh SW, Aoyama K, Chen Y, Garnier P, Matsumori Y, Gum E, Liu J, Swanson RA: Hypoglycemic neuronal death and cognitive impairment are prevented by poly(ADP-ribose) polymerase inhibitors administered after hypoglycemia. J Neurosci 2003, 23, 10681 –10690.
 
40.
Sumiyoshi T, Ichikawa J, Meltzer HY: The effect of streptozotocin-induced diabetes on dopamine2, serotonin1A and serotonin 2A receptors in the rat brain. Neuropsychopharmacology. 1997, 16 (3), 183-190.
 
41.
Tasaka Y, Matsumoto H, Inoue Y, Hirata Y: Brain catecholamine concentrations in hyperosmolar diabetic and diabetic rats. Diabetes Res. 1992, 19 (1), 1-7.
 
42.
Trimble LA, Sundberg, Markham L, Janicijevic S, Beattie BL, Meneilly GS: Value of the Clock Drawing Test to Predict Problems With Insulin Skills in Older Adults. Can J Diabetes. 2005, 29 (2), 102-103.
 
43.
Watson GS, Craft S: Modulation of memory by insulin and glucose: neuropsychological observations in Alzheimer's disease. Eur J Pharmacol. 2004, 490 (1-3), 97-113.
 
44.
Weingartner H, Rudorfer MV, Buchsbaum MS, Linnoila M: Effects of serotonin on memory impairments produced by ethanol. Science. 1983, 221 (4609), 472-474.
 
45.
Willis T: Pharmaceutice Rationalis (1684). In: The works of Thomas Willis. London: Dring Harpur & Lee, 1979, 74.
 
46.
Zhao WQ, Chen H, Quon MJ, Alkon DL: Insulin and the insulin receptor in experimental models of learning and memory. Eur J Pharmacol. 2004, 490 (1-3), 71-81.
 
eISSN:2084-4905
ISSN:2083-4543