Inflamasi dalam Patologi Penyaki Alzheimer

Penulis

  • Jan S. Purba Department of Neurology, Faculty of Medicine, Universitas Indonesia Jakarta

DOI:

https://doi.org/10.56951/medicinus.v33i3.70

Kata Kunci:

penyakit Alzheimer, β-amyloid, inflamasi, katarak

Abstrak

Penderita penyakit Alzheimer di tahun 2006 di seluruh dunia berjumlah sekitar 26,6 juta penduduk. Angka ini diperkirakan akan meningkat menjadi empat kali lipat di tahun 2050 sehubungan dengan angka harapan hidup yang meningkat di beberapa negara di dunia. Perjalanan penyakit Alzheimer berhubungan erat dengan proses akumulasi β-amyloid (Aβ) penyebab formasi neurofibrillary tangles (NFT) serta degenerasi sinapsis. Selain itu penumpukan Aβ menyebabkan peningkatan produksi faktor proinflamasi disertai aktivasi complement cascade yang berkontribusi terhadap respons inflamasi lokal. Komponen Aβ yang ditemukan di otak penderita Alzheimer juga ditemukan di lensa dan cairan mata. Protein ini diduga mengakibatkan jenis katarak yang berbeda dengan kebanyakan kasus katarak. Studi epidemiologi klinis menunjukkan bahwa terdapat penurunan prevalensi penyakit Alzheimer melalui pengobatan jangka panjang menggunakan obat antiinflamasi nonsteroid (OAINS). Di sisi lain dikatakan bahwa neuronal-type nicotinic acetylcholine receptors (nAChRs) dan peroxisomal proliferator-activated receptors (PPARs) juga berperan dalam proses patologi penyakit Alzheimer di otak, sehingga kedepannya strategi penanggulangan penyakit Alzheimer akan juga berfokus pada keterlibatan dan gangguan pada reseptor tersebut.

Referensi

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association;1994.

Petersen RC, Smith GE, Kokmen E. Mild cognitive impairment. Clinical characterization and outcome. Arch Neurol 1999;46:303-8. DOI: https://doi.org/10.1001/archneur.56.3.303

Palmer K, Wang HX, Backman L, Winglad B, Fratiglioni L. Differential evolution of cognitive impairment in nondemented older person: results from the Kungsdholmen Project. Am J Psychiatry 2002;159:436-42. DOI: https://doi.org/10.1176/appi.ajp.159.3.436

Wolf H, Grundwald M, Ecke GM, et al. The prognosis to mild cognitive impairment in the elderly. J Neural Transm Supp 1998;54:31-50. DOI: https://doi.org/10.1007/978-3-7091-7508-8_4

Di Carlo A, Baldereschi A, Amaducci L, et al. Cognitive impairment without dementia in older people: prevalence, vascular risk factors, impact on disability. The Italian Longitudinal Study on Aging. J Am Geriatr Soc 2000;48:775-82. DOI: https://doi.org/10.1111/j.1532-5415.2000.tb04752.x

Kivipelto M, Helkala EL, Hanninen T, et al. Midlife vascular risk factors and late-life mild cognitive impairment. A population-based study. Neurology 2001;56:1683-89. DOI: https://doi.org/10.1212/WNL.56.12.1683

Ficker C, Ferris SH, Reisberg B. Mild cognitive impairment in the elderly predictors of dementia. Neurology 1991;41:1006-9. DOI: https://doi.org/10.1212/WNL.41.7.1006

Gilmore GC, Whitehouse PJ. Contrast sensitivity in Alzheimer’s disease: a 1-year longitudinal analysis. Optom Vis Sci 1995;72:83–91.

Mendez MF, Cherrier MM, Meadows RS. Depth perception in Alzheimer’s disease. Percept Mot Skills 1996;83:987–95. DOI: https://doi.org/10.2466/pms.1996.83.3.987

Trick GL, Trick LR, Morris P, Wolf M. Visual field loss in senile dementia of the Alzheimer’s type. Neurology 1995;45:68-74. DOI: https://doi.org/10.1212/WNL.45.1.68

Gao S, Hendrie HC, Hall KS, Hui S. The relationships between age, sex, and the incidence ofdementia and Alzheimer disease: a meta-analysis. Arch Gen Psychiatry 1998;55:809-15. DOI: https://doi.org/10.1001/archpsyc.55.9.809

Brookmeyer R, Johnson E, Ziegler-Graham K, Arrighi HM. Forecasting the global burden of Alzheimer’s disease. Alzheimers Dement. 2007;3:186-91. DOI: https://doi.org/10.1016/j.jalz.2007.04.381

Lobo A, Launer LJ, Fratiglioni L, et al. Prevalence of dementia and major subtypes in Europe: A collaborative study of population-based cohorts. Neurology 2000;54:S4-9.

Plassman BL, Langa KM, Fisher GG, et al. Prevalence of dementia in the United States: the aging, demographics, and memory study. Neuroepidemiology 2007;29:125-32. DOI: https://doi.org/10.1159/000109998

Ferri CP, Prince M. Brayne C, et al. Global prevalence of dementia: a Delphi consensus study. Lancet 2005;366:2112-7. DOI: https://doi.org/10.1016/S0140-6736(05)67889-0

Wimo A, Winblad B, Agüero-Torres H, von Strauss E. The magnitude of dementia occurrence in the world. Alzheimer Dis Assoc Disord. 2003;17:63-7. DOI: https://doi.org/10.1097/00002093-200304000-00002

Kalaria RN, Maestre GE, Arizaga R, et al. Alzheimer’s disease and vascular dementia in developing countries: prevalence, management, and risk factors. Lancet Neurol. 2008;7:812-26. DOI: https://doi.org/10.1016/S1474-4422(08)70169-8

Zhang ZX, Zahner GE, Roman GC, et al. Dementia subtypes in China: prevalence in Beijing, Xian, Shanghai, and Chengdu. Arch Neurol. 2005;62:447-53. DOI: https://doi.org/10.1001/archneur.62.3.447

Scazufca M, Menezes PR, Vallada HP, et al. High prevalence of dementia among older adults from poor socioeconomic backgrounds in São Paulo, Brazil. Int Psychogeriatr. 2008;20:394-405. DOI: https://doi.org/10.1017/S1041610207005625

Llibre Rodríguez J, Valhuerdi A, Sanchez II, et al. The prevalence, correlates and impact of dementia in Cuba: a 10/66 group population-based survey. Neuroepidemiology 2008;31:243-51. DOI: https://doi.org/10.1159/000165362

Tobinick E, Gross H, Weinberger A, Cohen H. TNF-alpha Modulation for Treatment of Alzheimer's Disease: A 6-Month Pilot Study. Medscape General Medicine 2006;8:25

Tan ZS, Beiser AS, Vasan RS, et al. Inflammatory markers and the risk of Alzheimer disease: the Framingham Study. Neurology 2008;70:1222-3. DOI: https://doi.org/10.1212/01.wnl.0000307660.86647.7b

McEwen BS. Effects of adverse experiences for brain structure and function. Biol Psychiatry 2000;48:721-31. DOI: https://doi.org/10.1016/S0006-3223(00)00964-1

Mullan M. Familial Alzheimer's disease: second gene locus located. BMJ 1992;305:1108-9. DOI: https://doi.org/10.1136/bmj.305.6862.1108

Palmer K, Berger AK, Monastero R, Windblad B, Baeckman L, Fratilioni L. Predictors of progression from mild cognitive impairment to Alzheimer disease. Neurology 2007;68:1596-602. DOI: https://doi.org/10.1212/01.wnl.0000260968.92345.3f

Schellenberg GD, Boehnke M, Wijsman EM, et al. Genetic association and linkage analysis of the locus and familial Alzheimer's disease. Ann Neurol 1992;31:223-7. DOI: https://doi.org/10.1002/ana.410310214

Koffie RM, Meyer-Luehmann M, Hashimoto T, et al. Oligomeric amyloid beta associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques. Proceed Nat Acad Sci 2009;106:4012-7. DOI: https://doi.org/10.1073/pnas.0811698106

Serrano-Pozo A, Frosch MP, Masliah E, Hyman BT. Neuropathological alterations in Alzheimer disease. Cold Spring Harb Perspect Med doi: 10.1101/cshperspect, 2011. DOI: https://doi.org/10.1101/cshperspect.a006189

Abramov E, Dolev I, Fogel H, Ciccotosto GD, Ruff E and Slutsky I. Amyloid- as a positive endogenous regulator of release probability at hippocampal synapses. Nature Neuroscience 2009;12:1567-76. DOI: https://doi.org/10.1038/nn.2433

Querfurth HW, LaFerla FM. Alzheimer's disease. N Engl J Med 2010;362:329-44. DOI: https://doi.org/10.1056/NEJMra0909142

Panza F, Solfrizzi V, Frisardi V, et al. Beyond the neurotransmitter-focused approach in treating Alzheimer's disease: drugs targeting beta-amyloid and tau protein. Aging Clin Exp Res 2009;21:386-406. DOI: https://doi.org/10.1007/BF03327445

Braak H, Braak E, Bohl J. Staging of Alzheimer-related cortical destruction. Eur Neurol. 1993;33:403–8. DOI: https://doi.org/10.1159/000116984

Heinonen O, Soininen H, Sorvari H, et al. Loss of synaptophysin-like immunoreactivity in the hippocampal formation is an early phenomenon in Alzheimer's disease. Neuroscience 1995;64: 375–84. DOI: https://doi.org/10.1016/0306-4522(94)00422-2

Jellinger KA, Bancher C. AD neuropathology. Neurology 1996;46:1186–7. DOI: https://doi.org/10.1212/WNL.46.4.1186-c

Salminen A, Ojala J, Kauppinen A, Kaarniranta K, Suuronen T. Inflammation in Alzheimer's disease: amyloid-beta oligomers trigger innate immunity defence via pattern recognition receptors. Prog Neurobiol. 2009;87:181-94. DOI: https://doi.org/10.1016/j.pneurobio.2009.01.001

Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science 2002;297:353–6. DOI: https://doi.org/10.1126/science.1072994

Selkoe DJ. Alzheimer's disease: A central role for amyloid. J Neuropathol Exp Neurol 1994;53:438–47. DOI: https://doi.org/10.1097/00005072-199409000-00003

Wisniewski T, Ghiso J, Frangione B. Alzheimer's disease and soluble A beta. Neurobiol Aging 1994;15:143–52. DOI: https://doi.org/10.1016/0197-4580(94)90105-8

López-Hernández GY, Thinschmidt JS, Morain P, et al. Positive modulation of alpha7- nAChR responses in rat hippocampal interneurons to full agonists and the alpha-selective partial agents, 40H-GTS-21 and S 24795. Neuropharmacology 2009;56:821-30. DOI: https://doi.org/10.1016/j.neuropharm.2009.01.011

Graeber MB. Changing face of microglia. Science 2010;330:783-8. DOI: https://doi.org/10.1126/science.1190929

Fuhrmann M, Bittner T, Jung CK, et al. Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer's disease. Nat Neurosci 2010;13:411-3. DOI: https://doi.org/10.1038/nn.2511

Tahara K, Kim HD, Jin JJ, Maxwell JA, Li L, Fukuchi K. Role of toll-like receptor signalling in Abeta uptake and clearance. Brain 2006;129:3006 -19. DOI: https://doi.org/10.1093/brain/awl249

Tuppo EE, Arias HR. The role of inflammation in Alzheimer’s disease. Int J Biochem Cell Biol 2005;37:289-305. DOI: https://doi.org/10.1016/j.biocel.2004.07.009

Hayes A, Thaker U, Iwatsubo T, Pickering- Brown SM, Mann DM’ Pathological relationships between microglial cell activity and tau and amyloid beta protein in patients with Alzheimer’s disease. Neurosci Lett 2002;331:171–4. DOI: https://doi.org/10.1016/S0304-3940(02)00888-1

Tarkowski E, Liljeroth AM, Minthon L, Tarkowski A, Wallin A, Blennow K: Cerebral pattern of pro- and anti-inflammatory cytokines in dementias. Brain Res Bull 2003;61:255–60. DOI: https://doi.org/10.1016/S0361-9230(03)00088-1

Cunningham C, Campion S, Lunnon K, et al. Systemic inflammation induces acute behavioral and cognitive changes and accelerates neurodegenerative disease. Biol Psychiatry 2009;65:304–12. DOI: https://doi.org/10.1016/j.biopsych.2008.07.024

Forlenza OV, Diniz BS, Talib LL, et al. Increased Serum IL-1β Level in Alzheimer’s Disease and Mild Cognitive Impairment. Dement Geriatr Cogn Disord 2009;28:507-12. DOI: https://doi.org/10.1159/000255051

G C Gilmore GC and Whitehouse PJ. Contrast Sensitivity in Alzheimer's Disease: A 1-year Longitudinal Analysis. Optom Vis Sci 1995;72:83-91. DOI: https://doi.org/10.1097/00006324-199502000-00007

Javaid FZ, Brenton J, Guo L and Cordeiro MF.Visual and Ocular Manifestations of Alzheimer’s Disease and Their Use as Biomarkers for Diagnosis and Progression. Front Neurol. 2016;7:55. DOI: https://doi.org/10.3389/fneur.2016.00055

Rizzo JF, 3rd, Cronin-Golomb A, Growdon JH, et al. Retinocalcarine function in Alzheimer’s disease: a clinical and electrophysiological study. Arch Neurol 1992;49:93–101. DOI: https://doi.org/10.1001/archneur.1992.00530250097023

Armstrong RA. Visual field defects in Alzheimer’s disease patients may reflect differential pathology in the primary visual cortex. Optom Vis Sci 1996;73:677–82. DOI: https://doi.org/10.1097/00006324-199611000-00001

Goldstein LE, Muffat JA, Cherny RA. Cytosolic beta-amyloid deposition and supranuclear cataracts in lenses from people with Alzheimer's disease. Lancet 2003;361:1258-65. DOI: https://doi.org/10.1016/S0140-6736(03)12981-9

Berisha F, Feke GT, Trempe CL, McMeel JW, Schepens CL. Retinal Abnormalities in Early Alzheimer’s Disease. Invest Ophthal Visual Science 2007;48:2285-9. DOI: https://doi.org/10.1167/iovs.06-1029

Donnelly RJ, Friedhoff AJ, Beer B, Blume AJ, Vitek MP. Interleukin-1 stimulates the beta-amyloid precursor protein promoter. Cell Mol Neurobiol 1990;10:485-95. DOI: https://doi.org/10.1007/BF00712843

Kawas CH, Corrada MM, Brookmeyer R, et al. Visual memory predicts Alzheimer's disease more than a decade before diagnosis. Neurology 2003;60:1089-93. DOI: https://doi.org/10.1212/01.WNL.0000055813.36504.BF

Hinton DR, Sadun AA, Blanks JC, Miller CA. Optic-nerve degeneration in Alzheimer’s disease. N Engl J Med 1986;315:485–7. DOI: https://doi.org/10.1056/NEJM198608213150804

Wostyn P, K Audenaert K, De Deyn PP. Alzheimer’s disease and glaucoma: Is there a causal relationship? Br J Ophthalmol 2009;93:1557-9. DOI: https://doi.org/10.1136/bjo.2008.148064

Blennow K, Hampel H, Weiner M, Zetterberg H. Cerebrospinal fluid and plasma biomarkers in Alzheimer disease. Nat Rev Neurol 2010;6:131-44. DOI: https://doi.org/10.1038/nrneurol.2010.4

Samgard K, Zetterberg H, Blennow K, Hansson O, Minthon L, Londos E. Cerebrospinal fluid total tau as a marker of Alzheimer's disease intensity. Int J Geriatr Psychiatry 2010;25:403-10. DOI: https://doi.org/10.1002/gps.2353

Blom ES, Giedraitis V, Zetterberg H, et al. Rapid progression from mild cognitive impairment to Alzheimer's disease in subjects with elevated levels of tau in cerebrospinal fluid and the APO epsilon4/epsilon4 genotype. Dement Geriatr Cogn Disord 2009;27:458-64. DOI: https://doi.org/10.1159/000216841

Buerger K, Ewers M, Andreasen N, et al. Phosphorylated tau predicts rate of cognitive decline in MCI subjects: a comparative CSF study. Neurology 2005;65:1502-3. DOI: https://doi.org/10.1212/01.wnl.0000183284.92920.f2

Buerger K, Ewers M, Pirttilä T, et al. CSF phosphorylated tau protein correlates with neocortical neurofibrillary pathology in Alzheimer's disease. Brain 2006;129:3035-41. DOI: https://doi.org/10.1093/brain/awl269

Tapiola T, Alafuzoff I, Herukka SK, et al. Cerebrospinal fluid {beta}-amyloid 42 and tau proteins as biomarkers of Alzheimer-type pathologic changes in the brain. Arch Neurol 2009;66:382-89. DOI: https://doi.org/10.1001/archneurol.2008.596

Fagan AM, Mintun MA, Mach RH, et al. Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Abeta42 in humans. Ann Neurol 2006;59:512-9. DOI: https://doi.org/10.1002/ana.20730

Forsberg A, Engler H, Almkvist O, et al. PET imaging of amyloid deposition in patients with mild cognitive impairment. Neurobiol Aging 2008;29:1456-65. DOI: https://doi.org/10.1016/j.neurobiolaging.2007.03.029

Mattsson N, Zetterberg H. Future screening for incipient Alzheimer's disease-the influence of prevalence on test performance. Eur Neurol 2009;62:200-3. DOI: https://doi.org/10.1159/000228591

Solomon B. Immunological approaches as therapy for Alzheimer's disease. Expert Opin Biol Ther 2002;2:907-17. DOI: https://doi.org/10.1517/14712598.2.8.907

De Craen A.J., Gussekloo J., Vrijsen B, Westendorp RG. Meta-analysis of nonsteroidal antiinflammatory drug use and risk of dementia. Am J Epidemiol 2005;161:114-20. DOI: https://doi.org/10.1093/aje/kwi029

Douglas W, Lih-Fen L. Anti-inflammatory and Immune Therapy for Alzheimer's Disease: Current Status and Future Directions. Current Neuropharmacol 2007;5:232-43. DOI: https://doi.org/10.2174/157015907782793667

McGeer PL, McGeer EG. NSAIDs and Alzheimer disease: Epidemiological, animal model and clinical studies. Neurobiology of Aging 2007;28:639-47. DOI: https://doi.org/10.1016/j.neurobiolaging.2006.03.013

Lynch G. Memory and the brain: unexpected chemistries and a new pharmacology. Neurobiol Learn Mem 1998;70:82–100. DOI: https://doi.org/10.1006/nlme.1998.3840

Hampel H, Blennow K, Shaw LM, Hoessler YC, Zetterberg H, Trojanowski JQ. Total and phosphorylated tau protein as biological markers of Alzheimer's disease. Exp Gerontol 2010;45:30-40. DOI: https://doi.org/10.1016/j.exger.2009.10.010

Trojanowski JQ, Schuck T, Schmidt ML, Lee VM. Distribution of tau proteins in the normal human central and peripheral nervous system. J Histochem Cytochem 1989;37:209-15. DOI: https://doi.org/10.1177/37.2.2492045

Lovestone S, Reynolds CH. The phosphorylation of tau: a critical stage in neurodevelopment and neurodegenerative processes. Neuroscience 1997;78:309-24.

Diterbitkan

01-12-2020

Unduhan

Data unduhan tidak tersedia.

Cara Mengutip

[1]
Inflamasi dalam Patologi Penyaki Alzheimer. MEDICINUS 2020;33:65-71. https://doi.org/10.56951/medicinus.v33i3.70.