Zusammenfassung
Morbus Alzheimer ist eine neurodegenerative, progrediente und irreversible Erkrankung und die häufigste und bekannteste Demenzerkrankung. Zurzeit ist etwa 1% der deutschen Gesamtbevölkerung betroffen. Die Wahrscheinlichkeit an Alzheimer zu erkranken, steigt exponentiell mit dem Lebensalter. Auf Grund der höheren Lebenserwartung sind Frauen gegenüber Männern bisher mit einem Anteil von 7:3 deshalb stärker betroffen. Für das Jahr 2050 rechnet man mit einer Patientenzahl von 2,3 Millionen.
Die Krankheitsursachen sind nicht völlig geklärt. Es gibt einige seltene vererbte Fälle, der Mehrzahl der Erkrankungen liegen mehrere Ursachen/Lebensumstände zugrunde. Die Zelldegeneration, die über 10–30 Jahre dauert, findet in den tiefer liegenden Anteilen des Temporal- und Parietallappens und weniger im Frontallappen statt. Eine eindeutige Diagnose kann erst post mortem durch eine histopathologische Untersuchung des Gehirnbiopsats erfolgen.
Generell kommt es zu einem individuell stark unterschiedlichen Verlust der Merkfähigkeit und des Gedächtnisses. Aktuell steht eine symptomatische Therapie zur Verfügung. Acetylcholesterase-Hemmer und NMDA-Rezeptor-Antagonisten werden hierfür eingesetzt.
Präventiv scheinen eine ausgewogene Ernährung, körperliche Bewegung und geistige Aktivitäten zu wirken.
Abstract
Alzheimer’s Disease is a progressive, degenerative and irreversible brain disorder and the most widespread and well-known form of dementia. Currently 1% of the German population is affected. The risk to suffer from this disease increases with age. This is the reason why women, who generally live longer, are affected more often than men (7:3). Estimations for the year 2050 predict more than 2,3 millions patients.
The causes of AD are not fully understood. The disease course runs from ten to thirty years and affects mainly the parietal and the temporal lobe. There are some rare inherited cases, but for most cases there is an interaction of genetic, environmental and life-style risk factors, with age playing the largest part.
The rate and quality of decline varies from patient to patient. Clear proof of AD can only be obtained by examining the brain after death.
Drug treatment can relieve some symptoms such as cholinesterase inhibitors including donezepil, galantamine and rivastigmine or NMDA receptor antagonist (memantine).
A well-balanced diet, regular physical and mental exercises play an important role in prevention.
Literaturverzeichnis
Ballenger JF, Nelson JL, Whitehouse PJ (1999). Beyond „progress“ in the history of Alzheimer disease. Alzheimer Dis Assoc Disord 13: 130–131
Bertoni-Freddari C, Fattoretti P, Casoli T, Meier-Ruge W, Ulrich J (1990). Morphological adaptive response of the synaptic junctional zones in the human dentate gyrus during aging and Alzheimer’s disease. Brain Res 517: 69–75
Bickel H (2000). [Dementia syndrome and Alzheimer disease: an assessment of morbidity and annual incidence in Germany]. Gesundheitswesen 62: 211–218
Bosboom JL, Stoffers D, Wolters E (2004). Cognitive dysfunction and dementia in Parkinson’s disease. J Neural Transm 111: 1303–1315
Braak H, Braak E (1991). Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol 82: 239–259
Buch K, Riemenschneider M, Bartenstein P, Willoch F, Muller U, Schmolke M, Nolde T, Steinmann C, Guder WG, Kurz A (1998). [Tau protein. A potential biological indicator for early detection of Alzheimer disease]. Nervenarzt 69: 379–385
Campion D, Dumanchin C, Hannequin D, Dubois B, Belliard S, Puel M, Thomas-Anterion C, Michon A, Martin C, Charbonnier F, Raux G, Camuzat A, Penet C, Mesnage V, Martinez M, Clerget-Darpoux F, Brice A, Frebourg T (1999). Early-onset autosomal dominant Alzheimer disease: prevalence, genetic heterogeneity, and mutation spectrum. Am J Hum Genet 65: 664–670
Chagnon P, Betard C, Robitaille Y, Cholette A, Gauvreau D (1995). Distribution of brain cytochrome oxidase activity in various neurodegenerative diseases. Neuroreport 6: 711–715
Chang JB, Wang PN, Chen WT, Liu CY, Hong CJ, Lin KN, Liu TY, Chi CW, Liu HC (2004). ApoE epsilon4 allele is associated with incidental hallucinations and delusions in patients with AD. Neurology 63: 1105–1107
Colliot O, Chetelat G, Chupin M, Desgranges B, Magnin B, Benali H, Dubois B, Garnero L, Eustache F, Lehericy S (2008). Discrimination between Alzheimer disease, mild cognitive impairment, and normal aging by using automated segmentation of the hippocampus. Radiology 248: 194–201
Corbo RM, Scacchi R (1999). Apolipoprotein E (APOE) allele distribution in the world. Is APOE*4 a ‘thrifty’ allele? Ann Hum Genet 63: 301–310
Dal Forno G, Carson KA, Brookmeyer R, Troncoso J, Kawas CH, Brandt J (2002). APOE genotype and survival in men and women with Alzheimer’s disease. Neurology 58: 1045–1050
Davis RE, Miller S, Herrnstadt C, Ghosh SS, Fahy E, Shinobu LA, Galasko D, Thal LJ, Beal MF, Howell N, Parker WD, Jr. (1997). Mutations in mitochondrial cytochrome c oxidase genes segregate with late-onset Alzheimer disease. Proc Natl Acad Sci U S A 94: 4526–4531
de Leonni Stanonik M, Licata CA, Walton NC, Lounsbury JW, Hutson RK, Dougherty JH, Jr. (2005). The Self Test: a screening tool for dementia requiring minimal supervision. Int Psychogeriatr 17: 669–678
DeKosky ST, Scheff SW (1990). Synapse loss in frontal cortex biopsies in Alzheimer’s disease: correlation with cognitive severity. Ann Neurol 27: 457–464
Derouesne C (2008). [Alzheimer and Alzheimer’s disease: the present enlighted by the past. An historical approach]. Psychol Neuropsychiatr Vieil 6: 115–128
Evans DA (1996). The epidemiology of dementia and Alzheimer’s disease: an evolving field. J Am Geriatr Soc 44: 1482–1483
Finckh U, Muller-Thomsen T, Mann U, Eggers C, Marksteiner J, Meins W, Binetti G, Alberici A, Hock C, Nitsch RM, Gal A (2000). High prevalence of pathogenic mutations in patients with early-onset dementia detected by sequence analyses of four different genes. Am J Hum Genet 66: 110–117
Garrard P, Patterson K, Watson PC, Hodges JR (1998). Category specific semantic loss in dementia of Alzheimer’s type. Functional-anatomical correlations from cross-sectional analyses. Brain 121(Pt 4): 633–646
Giacobini E (2004). Cholinesterase inhibitors: new roles and therapeutic alternatives. Pharmacol Res 50: 433–440
Glenner GG, Wong CW, Quaranta V, Eanes ED (1984). The amyloid deposits in Alzheimer’s disease: their nature and pathogenesis. Appl Pathol 2: 357–369
Gotz J, Chen F, van Dorpe J, Nitsch RM (2001). Formation of neurofibrillary tangles in P301l tau transgenic mice induced by Abeta 42 fibrils. Science 293: 1491–1495
Graeber MB, Mehraein P (1999). Reanalysis of the first case of Alzheimer’s disease. Eur Arch Psychiatry Clin Neurosci 249Suppl 3: 10–13
Haass C, Schlossmacher MG, Hung AY, Vigo-Pelfrey C, Mellon A, Ostaszewski BL, Lieberburg I, Koo EH, Schenk D, Teplow DB, et al. (1992). Amyloid beta-peptide is produced by cultured cells during normal metabolism. Nature 359: 322–325
Hampel H, Teipel SJ, Padberg F, Haslinger A, Riemenschneider M, Schwarz MJ, Kotter HU, Scheloske M, Buch K, Stubner S, Dukoff R, Lasser R, Muller N, Sunderland T, Rapoport SI, Moller HJ (1999). Discriminant power of combined cerebrospinal fluid tau protein and of the soluble interleukin-6 receptor complex in the diagnosis of Alzheimer’s disease. Brain Res 823: 104–112
Hebert LE, Scherr PA, McCann JJ, Beckett LA, Evans DA (2001). Is the risk of developing Alzheimer’s disease greater for women than for men? Am J Epidemiol 153: 132–136
Herholz K, Bauer B, Wienhard K, Kracht L, Mielke R, Lenz MO, Strotmann T, Heiss WD (2000). In-vivo measurements of regional acetylcholine esterase activity in degenerative dementia: comparison with blood flow and glucose metabolism. J Neural Transm 107: 1457–1468
Hippius H, Muller N (2008). The work of Emil Kraepelin and his research group in Munchen. Eur Arch Psychiatry Clin Neurosci 258Suppl 2: 3–11
Hock C, Nitsch RM (2000). [Alzheimer dementia]. Praxis (Bern 1994) 89: 529–540
Hoyer S (1995). Age-related changes in cerebral oxidative metabolism. Implications for drug therapy. Drugs Aging 6: 210–218
Hoyer S, Frölich L, Sandbrink R. Molekulare Medizin der Alzheimer-Krankheit. In: Ganten D, Ruckpaul K, ed, Erkrankungen des Zentralnervensystems Handbuch der molekularen Medizin. Berlin Heidelberg New York: Springer: 1999: 195–236
Hulstaert F, Blennow K, Ivanoiu A, Schoonderwaldt HC, Riemenschneider M, De Deyn PP, Bancher C, Cras P, Wiltfang J, Mehta PD, Iqbal K, Pottel H, Vanmechelen E, Vanderstichele H (1999). Improved discrimination of AD patients using beta-amyloid(1–42) and tau levels in CSF. Neurology 52: 1555–1562
Jagger C, Andersen K, Breteler MM, Copeland JR, Helmer C, Baldereschi M, Fratiglioni L, Lobo A, Soininen H, Hofman A, Launer LJ (2000). Prognosis with dementia in Europe: A collaborative study of population-based cohorts. Neurologic Diseases in the Elderly Research Group. Neurology 54: S16–20
Janssen JC, Beck JA, Campbell TA, Dickinson A, Fox NC, Harvey RJ, Houlden H, Rossor MN, Collinge J (2003). Early onset familial Alzheimer’s disease: Mutation frequency in 31 families. Neurology 60: 235–239
Jellinger KA, Bancher C (1998). Neuropathology of Alzheimer’s disease: a critical update. J Neural Transm Suppl 54: 77–95
Kropp S, Zerr I, Schulz-Schaeffer WJ, Riedemann C, Bodemer M, Laske C, Kretzschmar HA, Poser S (1999). Increase of neuron-specific enolase in patients with Creutzfeldt-Jakob disease. Neurosci Lett 261: 124–126
Launer LJ, Andersen K, Dewey ME, Letenneur L, Ott A, Amaducci LA, Brayne C, Copeland JR, Dartigues JF, Kragh-Sorensen P, Lobo A, Martinez-Lage JM, Stijnen T, Hofman A (1999). Rates and risk factors for dementia and Alzheimer’s disease: results from EURODEM pooled analyses. EURODEM Incidence Research Group and Work Groups. European Studies of Dementia. Neurology 52: 78–84
Lindsay J, Laurin D, Verreault R, Hebert R, Helliwell B, Hill GB, McDowell I (2002). Risk factors for Alzheimer’s disease: a prospective analysis from the Canadian Study of Health and Aging. Am J Epidemiol 156: 445–453
Iino M, Goto K, Kakegawa W, Okado H, Sudo M, Ishiuchi S, Miwa A, Takayasu Y, Saito I, Tsuzuki K, Ozawa S (2001). Glia-synapse interaction through Ca2+-permeable AMPA receptors in Bergmann glia. Science 292: 926–929
Maas D, Jochen A, Lalande B (1997). Age-related changes in male gonadal function. Implications for therapy. Drugs Aging 11: 45–60
Martins CA, Oulhaj A, de Jager CA, Williams JH (2005). APOE alleles predict the rate of cognitive decline in Alzheimer disease: a nonlinear model. Neurology 65: 1888–1893
Meier-Ruge W, Bertoni-Freddari C, Iwangoff P (1994). Changes in brain glucose metabolism as a key to the pathogenesis of Alzheimer’s disease. Gerontology 40: 246–252
Mori E, Lee K, Yasuda M, Hashimoto M, Kazui H, Hirono N, Matsui M (2002). Accelerated hippocampal atrophy in Alzheimer’s disease with apolipoprotein E epsilon4 allele. Ann Neurol 51: 209–214
Perl DP, Pendlebury WW (1986). Neuropathology of dementia. Neurol Clin 4: 355–368
Perry RJ, Watson P, Hodges JR (2000). The nature and staging of attention dysfunction in early (minimal and mild) Alzheimer’s disease: relationship to episodic and semantic memory impairment. Neuropsychologia 38: 252–271
Reiman EM, Caselli RJ (1999). Alzheimer’s disease. Maturitas 31: 185–200
Rogers SL, Doody RS, Pratt RD, Ieni JR (2000). Long-term efficacy and safety of done-pezil in the treatment of Alzheimer’s disease: final analysis of a US multicentre open-label study. Eur Neuropsychopharmacol 10: 195–203
Saunders AM, Strittmatter WJ, Schmechel D, George-Hyslop PH, Pericak-Vance MA, Joo SH, Rosi BL, Gusella JF, Crapper-MacLachlan DR, Alberts MJ, et al. (1993). Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer’s disease. Neurology 43: 1467–1472
Scarmeas N, Brandt J, Albert M, Devanand DP, Marder K, Bell K, Ciappa A, Tycko B, Stern Y (2002). Association between the APOE genotype and psychopathologic symptoms in Alzheimer’s disease. Neurology 58: 1182–1188
Scheff SW, Price DA (1993). Synapse loss in the temporal lobe in Alzheimer’s disease. Ann Neurol 33: 190–199
Scheuner D, Eckman C, Jensen M, Song X, Citron M, Suzuki N, Bird TD, Hardy J, Hutton M, Kukull W, Larson E, Levy-Lahad E, Viitanen M, Peskind E, Poorkaj P, Schellenberg G, Tanzi R, Wasco W, Lannfelt L, Selkoe D, Younkin S (1996). Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer’s disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer’s disease. Nat Med 2: 864–870
Schnider A (2001). Spontaneous confabulation, reality monitoring, and the limbic system—a review. Brain Res Brain Res Rev 36: 150–160
Schwalen S, Forstl H (2008). [Alzheimer’s disease: knowledge and attitudes in a representative survey]. Neuropsychiatr 22: 35–37
Seubert P, Oltersdorf T, Lee MG, Barbour R, Blomquist C, Davis DL, Bryant K, Fritz LC, Galasko D, Thal LJ, et al. (1993). Secretion of beta-amyloid precursor protein cleaved at the amino terminus of the beta-amyloid peptide. Nature 361: 260–263
Silverman JM, Raiford K, Edland S, Fillenbaum G, Morris JC, Clark CM, Kukull W, Heyman A (1994). The Consortium to Establish a Registry for Alzheimer’s Disease (CERAD). Part VI. Family history assessment: a multicenter study of first-degree relatives of Alzheimer’s disease probands and nondemented spouse controls. Neurology 44: 1253–1259
Silverman JM, Smith CJ, Marin DB, Mohs RC, Propper CB (2003). Familial patterns of risk in very late-onset Alzheimer disease. Arch Gen Psychiatry 60: 190–197
Sommers MS, Huff LM (2003). The effects of age and dementia of the Alzheimer’s type on phonological false memories. Psychol Aging 18: 791–806
Tiraboschi P, Hansen LA, Masliah E, Alford M, Thal LJ, Corey-Bloom J (2004). Impact of APOE genotype on neuropathologic and neurochemical markers of Alzheimer disease. Neurology 62: 1977–1983
van Duijn CM, Clayton D, Chandra V, Fratiglioni L, Graves AB, Heyman A, Jorm AF, Kokmen E, Kondo K, Mortimer JA, et al. (1991). Familial aggregation of Alzheimer’s disease and related disorders: a collaborative re-analysis of case-control studies. EURODEM Risk Factors Research Group. Int J Epidemiol 20Suppl 2: S13–20
Whitmer RA, Sidney S, Selby J, Johnston SC, Yaffe K (2005). Midlife cardiovascular risk factors and risk of dementia in late life. Neurology 64: 277–281
Winblad B, Poritis N (1999). Memantine in severe dementia: results of the 9M-Best Study (Benefit and efficacy in severely demented patients during treatment with memantine). Int J Geriatr Psychiatry 14: 135–146
Wolfson C, Wolfson DB, Asgharian M, M’Lan CE, Ostbye T, Rockwood K, Hogan DB (2001). A reevaluation of the duration of survival after the onset of dementia. N Engl J Med 344: 1111–1116
Zerr I, Bodemer M, Gefeller O, Otto M, Poser S, Wiltfang J, Windl O, Kretzschmar HA, Weber T (1998). Detection of 14-3-3 protein in the cerebrospinal fluid supports the diagnosis of Creutzfeldt-Jakob disease. Ann Neurol 43: 32–40
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Tropp, S., Vitzthum, K., Mache, S. et al. Morbus Alzheimer — Epidemiologie, Diagnose und Therapie. Zbl Arbeitsmed 60, 92–99 (2010). https://doi.org/10.1007/BF03344264
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DOI: https://doi.org/10.1007/BF03344264