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2014 | 4 | 6 | 57-70
Article title

Comorbidities disorders and Alzheimer's disease

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EN
Zaburzenia i schorzenia współistniejące z chorobą Alzheimera
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EN
Abstracts
EN
Abstract
Introduction. Alzheimer's disease is a chronic, progressive, neurodegenerative disease of the brain initially runs with disorders of higher cortical function, leading to dementia and a complete failure. Among the most important modifiable risk factors stand out: advanced age, genetic predisposition towards dementia and sex.Ch Orob Alzheimer's disease is heterogeneous in terms of clinical, neuropathological, biochemical and molecular level, can take place accompanied by a number of disorders and disease entities.
Purpose. Presentation and discussion of disorders, and comorbidity of Alzheimer's disease.
Materials and methods. Using a key Alzheimer's disease (Alzheimer's disease), comorbidities (comorbidity) Polish and foreign searched electronic bibliographic databases: Polish Medical Bibliography, EBSCO Host Web, Wiley Online Library, Springer Link, Science Direct, Medline.
Results. Finally, analysis of the scientific reports showed that frequently co-existing disorders, and Alzheimer's disease include: disease entities associated with hypoestrogenemia, cognitive and behavioral deficits, depression, diabetes type 2, conversion of ocular disorders and eating habits, sleep, bladder control bladder and bowel, and sexual dysfunction.
Conclusions. A multitude of sickness characterized by Alzheimer's disease shows coercion interdisciplinary care for early diagnosis not only cognitive deficits but also often concomitant ophthalmic internal medicine, neurological and psychiatric disorders. = Streszczenie
Wstęp. Choroba Alzheimera to przewlekła, postępująca, pierwotnie neurodegeneracyjna choroba mózgu przebiegająca z zaburzeniami wyższych czynności korowych, prowadząca do otępienia i pełnej niesprawności. Wśród niemodyfikowalnych najważniejszych czynników ryzyka wyróżnia się: zaawansowany wiek, uwarunkowania genetyczne w kierunku otępienia oraz płeć. Choroba Alzheimera jest schorzeniem heterogennym pod względem klinicznym, neuropatologicznym, biochemicznym i molekularnym, może przebiegać w towarzystwie licznych zaburzeń oraz jednostek chorobowych.
Cel. Przedstawienie i omówienie zaburzeń oraz schorzeń współistniejących z chorobą Alzheimera.
Materiał i metody. Posługując się kluczowymi choroba Alzheimera (Alzheimer’s disease), choroby współistniejące (comorbidity) przeszukano polskie oraz zagraniczne elektroniczne bazy bibliograficzne: Polska Bibliografia Lekarska, EBSCO host Web, Wiley Online Library, Springer Link, Science Direct, Medline.
Wyniki. Ostatecznie analiza doniesień naukowych wykazała, że do często współistniejących z chorobą Alzheimera zaburzeń oraz schorzeń można zaliczyć: jednostki chorobowe związane z hipoestrogenizmem, deficyty poznawcze i behawioralne, depresje, cukrzyce typu 2, zamiany oczne, a także zaburzenia nawyków żywieniowych, snu, kontroli nad pęcherzem moczowym i jelitami oraz zaburzenia seksualne.
Wnioski. Mnogość chorobowa charakteryzująca chorobę Alzheimera ukazuje przymus opieki interdyscyplinarnej w celu wczesnego zdiagnozowania nie tylko deficytów poznawczych ale również często współistniejących okulistycznych, internistycznych, neurologicznych i psychiatrycznych zaburzeń.
Publisher

Year
Volume
4
Issue
6
Pages
57-70
Physical description
References
  • Bilikiewicz A. Psychiatria. Podręcznik dla studentów medycyny. wyd. lekarskie PZWL. Warszawa, 2006.
  • McKhann GM, Knopman DS, Chertkow H et al. The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer's disease. 2011:7; 261-265
  • Abrams WB, Beers MB, Berkow R. Podręcznik geriatrii. Wyd. medyczne Urban&Partner Wrocław, 1999, 12165-1218, 1224-1228, 1234-1249, 1286-1293.
  • Berkow R, Abrams WB, Beers MB. Podręcznik diagnostyki I terapii. Wyd. medyczne Urban&Partner, Wrocław, 1995, 1612-1623, 1638-1641, 1748-1754.
  • Ożarowski M, Kupsz J, Torlińska T. Biologiczne czynniki ryzyka choroby Alzheimera. Biological risk factor for Alzheimer disease. Nowiny lekarskie.2006: 75(2); 193-198.
  • Breteler MB, Ott A, Hofman A. et al. Vascular disease and vascular risk factor and dementia. Epidemiology of Alzheimer’s Disease.1999: 79-86.
  • Globe LJ. Proces neurodegeracji w dobie biologii molekularnej. BMJ wyd.pol. 2002: 12(100); 8-9.
  • Cotran RS, Cumar V, Collins T. Robbins patalogic basis of disease. Wyd. Raven Press. Philadelphia. 1999; 1322-1338.
  • Buttini M, Orth M. Expresion of Apolipoproteine E3 or E4 in the Brains of ApoE/ Mice: Izoform- specific effects on neurodegeneration. J.Neurology. 2001; 248: 255-259.
  • Haines CJ. Estrogeny a choroba Alzheimera. Wiadomości położniczo-ginekologiczne. 2000; 2 (20): 138- 150.
  • Tanzi RE, Bertran L. New frontiers of Alzheimer’s disease genetics. Neuron. 2001; 32(2):181-184.
  • Krzyczkowska- Sendrakowska M. Czy można przeciwdziałać starzeniu się kobiecego mózgu i rozwojowi choroby Alzheimera. Przegląd menozpauzalny. 2013; 1: 13-14.
  • Poutanen M. Understanding the diversity of sex steroid action. J Endocrinol 2012; 212: 1-2.
  • Arevalo Ma, Riuz- Palmero I, Scerbo MJ, at al. Molecular mechanism involved in the regulation of neuritogenesis by estradiol: Recent advances. J Steroid Biochem Mol Biol. 2012; 131: 2-9.
  • Patlak M. Protecting of aging wopmen’s brain. Endocrine news 2011.
  • Pertyński T, Stachowiak G. Menopause-facts and controversies. Endokrynoloia Polska. 2006; 57: 527-529.
  • Sobczuk A. Diagnostyka i leczenie nieprawidłowych krwawień z dróg rodnych u kobiet w okresie około- i pomenopauzalnym. Nowa Medycyna. 1998;15: 34–36.
  • Pschyrembel W, Strauss G, Petri E. Ginekologia Praktyczna. PZWL, Warszawa 1994.
  • Guinot C, Malvy D, Ambroisine L et al. Effect of hormone replacement therapy on cutaneous biophysical properties of menopausal women. Ann Dermatol Venerol. 2002;129: 1129-1131.
  • Riggs BL, Melton LJ III. Involutional osteoporosis. N EngI J Med 1986; 314: 1676-1680.
  • Dembińska- Kieć A. Gospodarka lipidowa w menopauzie. Pol Arch Wew. 1998; 100; 211-219.
  • Jensen M. Health consequences of fat distribution. Horm Res 1997; 48: 88-92.
  • Thom T, Haase N, Rosamond W et al. Heart Disease and Statistic- 2006 Update. A Repport From the American Heart Assotation Statistics Committeee and Stroke Statistics Sucommmittee. Circulation 2006; 113: 85 – 696.
  • Miller AB, Bullbrook RD. UICC Multidisciplinary Project on Breast Cancer. He epidemiology, etiology and preventions of breast cance. Unt J Cancer. 1986; 37:173.
  • Jarema M, Jabłońska JR. Psychiatria. Podręcznik dla studentów medycyny. Zaburzenia psychiczne wywołane organicznym uszkodzeniem ośrodkowego układu nerwowego. Warszawa. PZWL. 2011; 63-64.
  • Lyketsos CG, Olin J. Depression in Alzheimer’s disease: overview and treatment. Biol. Psychiatry 2002; 52: 243- 252.
  • Zubenko GS, Zubenko WN, McPherson S. et al. A collaborative study of the emergence and clinical features of the major depressive syndrome of Alzheimer’s disease. Am. J.Psychiatry. 2003; 160: 857-866.
  • Lyketsos CG, Steinberg M, Tschantz J. et al. Mental and behavioral disturbances in dementia. Am.J. Psychiatry. 2000; 157: 708-714.
  • Cryan JF, Leonard BE. 5-HT1A and beyond: the role of serotonin and its receptors in depression and the antidepressant response. Human Psychopharmacology. 2000;15: 113-135.
  • Sweet RA, Poolock BG, Sukonick DL. et al. The 5-HTTPR polymorphism confers liability to a combined phenotype of psychotic and aggressive behavior in Alzheimer disease. International Psychogeriatrics 2001; 13 (4): 401-409.
  • Tyler WJ, Alonso M, Bramham CR, Pozzo-Miller MD. From acquisition to consolidation: on the role of brain-derived neurotrophic factor signaling in hippocampal-dependent learning. Learn Mem. 2002; 9: 224-237.
  • Yamada K, Muzino M, Nabeshima T. Role for brain –derived neurotrophing factor in learning and memory. Life Sci. 2002; 70: 735-744.
  • Hock C, Heese K, Hulette C et al. Region-specyficneurotrophin imbalances in Alzheimer’s disease: decreased levels of brain derived neurotrophic factor in hippocampus and cortical areas. Arch. Neurol. 2000; 57: 846-851.
  • Forstl H, Burns A, Luther P. Clinical and neuropathologycalcerrelates of depression in Alzheimer’s disease. Psychol. Med. 1992; 22: 877-884.
  • Harwood DG, Baker WW, Ownby RL et al. Association between premormid history of depression and current depression in Alzheimer’s disease. J. Geriatr. Psychiatry Neurology. 1999; 12: 72-75.
  • Jatczak-Stańczyk A, Nowakowska K, Kocur J. Coexisting disease of cognitive impairment and depression in patients with organic brain damage. Geriatria. 2013; 7: 86-90.
  • Austin MP, Ross M, Murray C. O’Caroll R.E., Ebemeier K.P., Goodwin G.M., Cognitive function in major depression. Journal Affect. Disorders 1993; 25: 21-30.
  • Zubenko GS, Zubenko WN, McPherson S et al. A collaborative study of the emergence and clinical features of the major depressive syndrome of Alzheimer’s disease. Am. J.Psychiatry.2003, 160: 857-866.
  • Hauser SL, Harrison MD. Neurologia w medycynie klinicznej. Tom1. Wydanie II polskie. Lublin; Wydawnictwo Czelej Sp. z o.o. 2012: 350-370.
  • Marszałek M.: Cukrzyca typu 2 a choroba Alzheimera- jedna czy dwie choroby? Mechanizmy asocjacji. Postepy Hig Med. Dosw. 2013; 67: 653-671.
  • Huang CC, Chung CM, Leu HB et al. Diabetes Mellitus and the Risk of Alzheimer’s Disease: A Nationwide Population-Based Study. PLoS ONE. 2014; 9: 1-7.
  • Andreetto E, Yan LM, Caporale A et al. Dissecting the role of single regions of an IAPP mimic and IAPP in inhibition of Aβ40 amyloid formation and cytotoxicity. Chembiochem. 2011; 12: 1313-1322.
  • Ott A, Stolk RP, Van Harskamp F et al. Diabetes mellitus and the risk of dementia: the Rotterdam Study. Neurology. 1999; 53: 1937–1942.
  • Abdul-Rahman O, Sasvari-Szekely M., Ver A et al. Altered gene expression profiles in the hippocampus and prefrontal cortex of type 2 diabetic rats. BMC Genomics. 2012; 13: 81.
  • Hölscher C. Diabetes as a risk factor for Alzheimer’s disease: insulin signalling impairment in the brain as an alternative model of Alzheimer’s disease. Biochem. Soc. Trans. 2011; 39: 891-897.
  • Accardi G, Caruso C, Colonna-Romano G et al. Can Alzheimer disease be a form of type 3 diabetes? Rejuvenation Res. 2012; 15: 217-221.
  • Miklossy J, Qing H, Radenovic A et al.Beta amyloid and hyperphosphorylated tau deposits in the pancreas in type 2 diabetes. Neurobiol. Aging. 2010; 31: 1503-1515.
  • Baglioni S, Casamenti F, Bucciantini M et al. Prefibrillar amyloid aggregates could be generic toxins in higher organisms. J. Neurosci. 2006; 26: 8160-8167.
  • Lorenzo A, Yankner BA. Amyloid fibril toxicity in Alzheimer’s disease and diabetes. Ann. NY Acad. Sci. 1996; 777: 89-95.
  • Stefani M. Structural features and cytotoxicity of amyloid oligomers: implications in Alzheimer’s disease and other diseases with amyloid deposits. Prog. Neurobiol. 2012; 99: 226-245.
  • Jackson HM, Soto I, Graham LC et al. Clustering of transcriptional profiles identifies changes to insulin signaling as an early event in a mouse model of Alzheimer's disease. BMC Genomics. 2013; 14: 831.
  • Shah K, DeSilva S, Abbruscato T. The Role of Glucose Transporters in Brain Disease: Diabetes and Alzheimer’s Disease. Int. J. Mol. Sci. 2012; 1: 12629-12655.
  • Jagust WJ, Seab JP, Huesman RH et al. Diminished glucose transport in Alzheimer’s disease: Dynamic pet studies. J. Cereb. Blood Flow Metab. 1991; 11: 323–330.
  • Sanz CM, Hanaire H, Vellas BJ et al.Diabetes mellitus as a modulator of functional impairment and decline in Alzheimer’s disease. The Real.FR cohort. Diabetic Medicine. 2011; 29: 541-548.
  • van Harten B, de Leeuw FE, Weinstein HC et al. Brain imaging in patients with diabetes: a systematic review. Diabetes Care. 2006; 29: 2539–2548.
  • Baezner H, Blahak C, Poggesi A et al. Association of gait and balance disorders with age-related white matter changes: the LADIS study. Neurology. 2008; 70: 935– 942.
  • Krasodomska K, Lubiński W, Potemkowski A et al. Zmiany okulistyczne współistniejące z chorobą Alzheimera. Okulistyka. 2010; 2: 15-21.
  • Maryke N.Alzheimer’s disease and the eye. Eye Care View. 2009; 3: 16-19.
  • Krasodomska K, Lubiński W, Potemkowski A, Honczarenko K. Zmiany elektrofizjologiczne u pacjentów we wczesnym stadium choroby Alzheimera. Ann Acad Med Stetin. 2007; 53: 49-57.
  • Linnér E, Popovic V, Gottfries CG et al. The exfoliation syndrome in cognitive impairment of cerebrovascular or Alzheimer's type. Acta Ophthalmologica Scandinavica. 2001; 79: 283-285.
  • Beelke M, Sannita WG. Cholinergic function and dysfunction in the visual system. Methods Find Exp Clin Pharmacol. 2002; 24: 113-117.
  • Janciauskiene S, Krakau T. Alzheimer's peptide and serine proteinase inhibitors in glaucoma and exfoliation syndrome. Doc Ophthalmol. 2003; 106: 215-223.
  • Wostyn P, Audenaert K, De Deyn PP. Alzheimer’s disease and glaucoma: Is there a causal relationship?. Br J Ophthalmol, 2009; 93: 1557-1559.
  • Kurowska AK, Kamińska A, Izdebska J et al. Zespół pseudoeksfoliacji (PEX) – schorzenie ogólnoustrojowe. Klin Oczna. 2009; 111: 160-164.
  • Parisi V. Correlation between morphological and functional retinal impairment in patients affected by ocular hypertension, glaucoma, demyelinating optic neuritis and Alzheimer's disease. Semin Opthalmol, 2003; 18: 50-57.
  • Cumurcu T, Dorak F, Cumurcu BE et al. Is there any relation between pseudoexfoliation syndrome and Alzheimer's type dementia?. Semin Ophthalmol, 2013; 28: 224-229.
  • Cormack FK, Tovee M, Ballard C. Contrast sensitivity and visual acuity in patients with Alzheimer's disease. International Journal of Geriatric Psychiatry. 2000; 15: 614-620.
  • Holroyd S, Sheldon-Keller A. A study of visual hallucinations in Alzheimer’s Disease. Am J Geriatr Psychiatry. 1995; 3: 198-205.
  • White H, Pieper C, Schmader K, et al. Weight change in Alzheimer's disease. Journal of the American Geriatrics Society.1996; 44(3):265-272.
  • Wang PN, Yang CL, RD, Lin KN et al. Weight loss, nutritional status and physical activity in patients with Alzheimer’s Disease. Journal of Neurology. 2004; 251(3): 314-320.
  • Pączek L, Niemczyk M. Geriatria. wyd. Czelej 2009. 136, 328-329.
  • Stewart R, Masaki K, Xue QL et al. A 32-Year Prospective Study of Change in Body Weight and Incident Dementia, Arch Neurol. 2005; 62(1): 55-60.
  • Shatenstein B, Kergoat MJ, Nadon S. Anthropometric changes over 5 years in elderly Canadians by age, gender, and cognitive status. J Gerontol A BiolSci Med Sci. 2001; 56 (8): 483-488.
  • DHS Oregon Department of Human Services. Alzheimer Diesese. 2012. [dostęp: 05.05.2014] http://www.oregon.gov/dhs/apd-dd training/EQC%20Training%20Documents/Alzheimer%27s%20Disease.pdf
  • Dunne TE, Neargarderemail SA, Cipolloni PB et al. Visual contrast enhances food and liquid intake in advanced Alzheimer's disease. Clinical Nutrition. 2004; 23(4):533-538.
  • Bliwise DL. Sleep disorders in Alzheimer's disease and other dementias. Clinical Cornerstone. 2004; 6(1), suppl.:16–28.
  • Vitiello MV, Bliwise DL, Prinz PN. Sleep in Alzheimer's disease and the sundown syndrome. Neurology. 1992; 42(7), suppl.:83-94.
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bwmeta1.element.psjd-0c78a6b9-a774-4edf-8a22-0fd15bac8759
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