A Review on the Alzheimer Disease Animal Models and Retinal Degeneration
Keywords:
Alzheimer, Retinal DegradationAbstract
Alzheimer’s disease (AD) is a chronic neurodegen- erative disease, serving as the most common form of dementia among the elderly population. AD targets various neurological processes in humans such as the visual pathway and hence resulting in various forms of visual abnormalities. Several studies have reported the loss of retinal ganglion cells, reduced thickness of nerve fibre layers (NFL) and damage of the optic nerve head and fiber layers. These findings suggest a putative link between AD and visual function deficits.
As genetic defects have been found to be associated with AD, it is possible to experimentally mimic this condition in animal models. AD gene mutations discovered in human amyloid pre- cursor protein (APP), presenilin 1/2 (PS1/PS2) and microtubule- associated tau protein have been used to engineer AD animal models.
In this review, we discuss the underlying molecular mecha- nisms of AD in terms of amyloidogenesis and tauopathies, as well as explain the pathological changes leading to vision loss in AD patients. Subsequently, the biology of the genes/proteins which have a causative link to AD, including APP, PS1 and PS2 will be discussed. Several recent reports of retinal degeneration in AD transgenic mouse models are selected to examine the relationship between AD and visual disturbance. We believe that a well- established method to generate transgenic mice will enhance our understanding of AD pathology and its correlation with retinal degeneration, leading to possible detection and treatment methods for AD.
References
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[28] M. Rizzo and M. Nawrot, “Perception of movement and shape in alzheimer’s disease,” Brain, vol. 121, pp. 2259–2270, 1998.
[29] M. T. Vanier, P. Neuville, L. Michalik, and J. F. Launay, “Expression of specific tau exons in normal and tumoral pancreatic acinar ncells,” Journal of Cell Science, vol. 111, pp. 1419–1432, 1998.
[30] S. Perez, S. Lumayag, B. Kovacs, E. J. Mufson, and X. S., “B- amyloid deposition and functional impairment in the retina of the appswe ps1deltae9 transgenic mouse model of alzheimer’s disease,” Investigative Ophthalmology and Visual Science, vol. 50, pp. 793–800, 2009.
[31] N. Hirokawa, Y. Shiomura, and S. Okabe, “Tau proteins: the molecular structure and mode of binding on microtubules,” Journal of Cell Biology, vol. 107, pp. 1449–1459, 1988.
[32] A. U. Bayer, O. N. Keller, F. Ferrari, and K. P. Maag, “Association of glaucoma with neurodegenerative diseases with apoptotic cell death: Alzheimer’s disease and parkinson’s disease,” American Journal of Ophthalmology, vol. 133, pp. 135–137, 2002.
[33] T. A. Bayer and O. Wirths, “Review on the app/ps1ki mouse model: intraneuronal a-accumulation triggers axonopathy, neuron loss and work- ing memory impairment,” Genes, Brain and Behaviour, vol. 7, no. 1, pp. 6–11, 2008.
[34] D. D. Kurylo, S. Corkin, R. Dolan, J. F. Rizzo, S. Parker, and J. H. Growdon, “Broad-band visual capacities are not selectively impaired in alzheimer’s disease,” Neurobiology of Aging, vol. 15, pp. 305–311, 1994.
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[36] J. C. Blanks, S. Y. Schmidt, Y. Torigoe, K. V. Porrello, D. R. Hinton, and R. H. Blanks, “Retinal pathology in alzheimer’s disease. ii. regional neuron loss and glial changes in gcl,” Neurobiology of Aging, vol. 17, no. 93, pp. 385–395, 1996.
[37] S. E. Arnold, B. T. Hyman, J. Flory, A. R. Damasio, and G. W. V. Hoesen, “The topographical and neuroanatomical distribution of neu- rofibrillary tangles and neuritic plaques in the cerebral cortex of patients with alzheimer’s disease,” Cerebral Cortex, vol. 1, pp. 103–116, 1991.
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[39] C. A. Curcio and D. N. Drucker, “Retinal ganglion-cells in alzheimer’s disease and aging,” Annals of Neurology, vol. 33, pp. 248–257, 1993.
12 JOURNAL OF UNDERGRADUATE RESEARCH IN ALBERTA (JURA), VOL. 1, JULY 2011
[40] D.C.Davies,P.McCoubrie,B.Mcdonald,andK.A.Jobst,“Myelinated axon number in the optic-nerve is unaffected by alzheimer’s disease,” British Journal of Ophthalmology, vol. 79, pp. 596–600, 1995.
[41] A. Cronin-Golomb, “Vision in alzheimer’s disease,” Gerontologist, vol. 35, p. 370, 1995.
[42] S. Estermann, G. C. Daepp, K. Cattapan-Ludewig, M. Berkhoff, B. E. Frueh, and D. Goldblum, “Effect of oral donepezil on intraocular pressure in normotensive alzheimer patients,” Journal of Ocular Phar- macology and Therapeutics, vol. 22, pp. 62–67, 2006.
[43] A.Cronin-Golomb,S.Corkin,J.F.Rizzo,andC.J.,“Visualdysfunction in alzheimer’s disease: Relation to normal aging,” Annals of Neurology, vol. 29, pp. 41–52, 1991.
[44] A. Cronin-Golomb, S. Corkin, and J. H. Growdon, “Visual dysfunction predicts cognitive deficits in alzheimer’s disease,” Optometry and Vision Science, vol. 72, pp. 168–176, 1995.
[45] G.C.Cronin-Golomb,A.adGilmore,S.Neargarder,S.R.Morrison,and T. M. Laudate, “Enhanced stimulus strength improvesvisual cognition in aging and alzheimer’s disease,” Cortex, vol. 43, pp. 952–966, 2007.
[46] M. M. Mesulam, “A plasticity-based theory of the pathogenesis of alzheimer’s disease,” Annals of the New York Academy of Sciences, vol. 924, pp. 42–52, 2000.
[47] M. Rizzo, S. W. Anderson, J. Dawson, and M. Nawrot, “Vision and cognition in alzheimer’s disease,” Neuropsychologia, vol. 38, no. 8, pp. 1157–1169, 2000.
[48] C. Bouras, P. R. Hof, P. Giannakopoulos, J. P. Michel, and J. H. Morrison, “Regional distribution of neurofibrillary tangles and senile plaques in the cerebral-cortex of elderly patients – a quantitative- evaluation of a one-year autopsy population from a geriatric hospital,” Cerebral Cortex, vol. 4, pp. 138–150, 1994.
[49] M. A. Westerman, D. Cooper-Blacketer, A. Mariash, L. Kotilinek, T. Kawarabayashi, L. H. Younkin, G. A. Carlson, S. G. Younkin, and K. H. Ashe, “The relationship between abeta and memory in the tg2576 mouse model of alzheimer’s disease,” Journal of Neuroscience, vol. 22, pp. 1858–1867, 2002.
[50] Q. Guo, W. Fu, B. L. Sopher, M. W. Miller, C. B. Ware, G. M. Martin, and M. P. Mattson, “Increased vulnerability of hippocampal neurons to excitotoxic necrosis in presenilin-1 mutant knock-in mice,” Nature Medicine, vol. 5, pp. 101–106, 1999.
[51] N. Gupta and Y. H. Yu ̈cel, “Glaucoma as a neurodegenerative disease,” Current Opinion in Ophthalmology, vol. 18, pp. 110–114, 2007.
[52] S. Oddo, A. Caccamo, M. Kitazawa, B. P. Tseng, and F. M. LaFerla,
“Amyloid deposition precedes tangle formation in a triple transgenic model of alzheimer’s disease,” Neurobiology of Aging, vol. 24, pp. 1063– 1070, 2003.
[53] D. Morgan, D. M. Diamond, P. E. Gottschall, K. E. Ugen, C. Dickey, J. Hardy, K. Duff, P. Jantzen, G. DiCarlo, D. Wilcock, K. Connor, J. Hatcher, C. Hope, M. Gordon, and G. W. Arendash, “A-peptide vaccination prevents memory loss in an animal model of alzheimer’s disease,” Nature, vol. 408, pp. 982–985, 2000.
[2] V. Chandra, N. E. Bharucha, and B. S. Schoenberg, “Conditions associ- ated with alzheimer’s disease at death – case-control study,” Neurology, vol. 36, pp. 209–211, 1986.
[3] R. M. Dutescu, Q. X. Li, J. Crowston, C. L. Masters, and P. N. Baird, “Amyloid precursor protein processing and retinal pathology in mouse models of alzheimer’s disease,” Graefe’s Archive for Clinical and Experimental Ophthalmology, vol. 247, pp. 1213–1221, 2009.
[4] L. Guo, J. Duggan, and M. F. Cordeiro, “Alzheimer’s disease and retinal neurodegeneration,” Science, vol. 49, no. 11, pp. 5136–5143, 2010.
[5] J. C. Blanks, D. R. Hinton, A. A. Sadun, and C. A. Miller, “Retinal
ganglion cell degeneration in alzheimer’s disease,” Brain Research, vol.
501, pp. 364–372, 1989.
[6] J. C. Blanks, Y. Torigoe, D. R. Hinton, and R. H. Blanks, “Retinal pathol-
ogy in alzheimer’s disease. i. ganglion cell loss in foveal/parafoveal
retina,” Neurobiology of Aging, vol. 17, pp. 377–384, 1996.
[7] L. V. Kessing, A. G. Lopez, P. K. Andersen, and S. V. Kessing, “No increased risk of developing alzheimer disease in patients with
glaucoma,” Journal of Glaucoma, vol. 16, pp. 47–51, 2007.
[8] A. U. Bayer, F. Ferrari, and C. Erb, “High occurrence rate of glaucoma among patients with alzheimer’s disease,” European Neurology, vol. 47,
pp. 165–168, 2002.
[9] N. Gupta, A. L. C. Fong, and Y. H. Yucel, “Retinal tau pathology in
human glaucomas,” Canadian Journal of Ophthalmology, vol. 43, pp.
53–60, 2008.
[10] J. Hardy and D. J. Selkoe, “The amyloid hypothesis of alzheimer’s
disease: progress and problems on the road to therapeutics,” Science,
vol. 297, pp. 353–356, 2002.
[11] S. Lesne ́, M. T. Koh, L. Kotilinek, R. Kayed, C. G. Glabe, A. Yang,
M. Gallagher, and K. H. Ashe, “A specific amyloid-beta protein assem-
bly in the brain impairs memory,” Nature, vol. 440, pp. 352–357, 2006.
[12] Y. Yoshiyama, M. Higuchi, B. Zhang, S. Huang, N. Iwata, T. Saido, J. Maeda, T. Suhara, J. Trojanowski, and V. Lee, “Synapse loss and microglial activation precede tangles in a p301s tauopathy mouse
model,” Neuron, vol. 53, pp. 337–351, 2007.
[13] A. A. Sadun and C. J. Bassi, “Optic nerve damage in alzheimer’s
disease,” Ophthalmology, vol. 97, pp. 9–17, 1990.
[14] G. M. Shankar and S. Li, “Amyloid-beta protein dimers isolated directly
from alzheimer’s brains impair 101 synaptic plasticity and memory,”
Nature Medicine, vol. 14, pp. 837–842, 2008.
[15] V. Lee, M. Goedert, and J. Q. Trojanowski, “Neurodegenerative
tauopathies,” Annual Review of Neuroscience, vol. 24, pp. 1121–1159,
2001.
[16] A. Ning, J. Cui, E. To, K. H. Ashe, and J. Matsubara, “Amyloid-beta
deposits lead to retinal degeneration in a mouse model of alzheimer disease,” Investigative Ophthalmology and Visual Science, vol. 49, pp. 5136–5143, 2008.
[17] C. Duyckaerts, M. C. Potier, and B. Delatour, “Alzheimer disease models and human neuropathology: similarities and difference,” Acta Neuropathologica, vol. 115, pp. 5–38, 2008.
[18] C.S.Tsai,R.Ritch,andB.Schwartz,“Opticnerveheadandnervefiber layer in alzheimer’s disease,” Archives of Ophthalmology, vol. 109, pp. 199–204, 1991.
[19] I. Grundke-Iqbal, K. Iqbal, M. Quinlan, Y. C. Tung, M. S. Zaidi, and H. M. Wisniewski, “Microtubule-associated protein tau. a component of alzheimer paired helical filaments,” Journal of Biological Chemistry, vol. 261, pp. 6084–6089, 1986.
[20] K. Hsiao, P. Chapman, S. Nilsen, C. Eckman, Y. Harigaya, S. Younkin, F. Yang, and G. Cole, “Correlative memory deficits, abeta elevation, and amyloid plaques in transgenic mice,” Science, vol. 274, pp. 99–102, 1996.
[21] R. Brandt and G. Lee, “Functional organization of microtubule- associated protein tau. identification of regions which affect microtubule growth, nucleation, and bundle formation in vitro,” Journal of Biological Chemistry, vol. 268, pp. 3414–3419, 1993.
[22] ——,“Thebalancebetweentauprotein’smicrotubulegrowthandnucle- ation activities: implications for the formation of axonal microtubules,” Journal of Neurochemistry, vol. 61, pp. 997–1005, 1993.
[23] D. W. Cleveland, S. Y. Hwo, and M. W. Kirschner, “Physical and chem- ical properties of purified tau factor and the role of tau in microtubule assembly,” Journal of Molecular Biology, vol. 116, pp. 227–247, 1977.
[24] ——, “Purification of tau, a microtubule associated protein that induces assembly of microtubules from purified tubulin,” Journal of Molecular Biology, vol. 116, pp. 207–225, 1977.
[25] T. Kawarabayashi, L. H. Younkin, T. C. Saido, M. Shoji, K. H. Ashe, and S. G. Younkin, “Age dependent changes in brain, csf, and plasma amyloid beta protein in the tg2576 transgenic mouse model of alzheimer’s disease,” Journal of Neuroscience, vol. 21, pp. 372–381, 2001.
[26] F. Berisha, G. T. Feke, C. L. Trempe, W. McMeel, and C. L. Schep- ens, “Retinal abnormalities in early alzheimer’s disease,” Investigative Ophthalmology and Visual Science, vol. 48, no. 5, pp. 2285–2290, 2007.
[27] M. F. Mendez, M. A. Mendez, R. Martin, K. A. Smyth, and P. J. Whitehouse, “Complex visual disturbances in alzheimer’s disease,” Neurology, vol. 40, pp. 439–443, 1990.
[28] M. Rizzo and M. Nawrot, “Perception of movement and shape in alzheimer’s disease,” Brain, vol. 121, pp. 2259–2270, 1998.
[29] M. T. Vanier, P. Neuville, L. Michalik, and J. F. Launay, “Expression of specific tau exons in normal and tumoral pancreatic acinar ncells,” Journal of Cell Science, vol. 111, pp. 1419–1432, 1998.
[30] S. Perez, S. Lumayag, B. Kovacs, E. J. Mufson, and X. S., “B- amyloid deposition and functional impairment in the retina of the appswe ps1deltae9 transgenic mouse model of alzheimer’s disease,” Investigative Ophthalmology and Visual Science, vol. 50, pp. 793–800, 2009.
[31] N. Hirokawa, Y. Shiomura, and S. Okabe, “Tau proteins: the molecular structure and mode of binding on microtubules,” Journal of Cell Biology, vol. 107, pp. 1449–1459, 1988.
[32] A. U. Bayer, O. N. Keller, F. Ferrari, and K. P. Maag, “Association of glaucoma with neurodegenerative diseases with apoptotic cell death: Alzheimer’s disease and parkinson’s disease,” American Journal of Ophthalmology, vol. 133, pp. 135–137, 2002.
[33] T. A. Bayer and O. Wirths, “Review on the app/ps1ki mouse model: intraneuronal a-accumulation triggers axonopathy, neuron loss and work- ing memory impairment,” Genes, Brain and Behaviour, vol. 7, no. 1, pp. 6–11, 2008.
[34] D. D. Kurylo, S. Corkin, R. Dolan, J. F. Rizzo, S. Parker, and J. H. Growdon, “Broad-band visual capacities are not selectively impaired in alzheimer’s disease,” Neurobiology of Aging, vol. 15, pp. 305–311, 1994.
[35] F. M. LaFerla, K. N. Green, and S. Oddo, “Intracellular amyloid-beta in alzheimer’s disease,” Nature Reviews Neuroscience, vol. 8, no. 98, pp. 499–509, 2007.
[36] J. C. Blanks, S. Y. Schmidt, Y. Torigoe, K. V. Porrello, D. R. Hinton, and R. H. Blanks, “Retinal pathology in alzheimer’s disease. ii. regional neuron loss and glial changes in gcl,” Neurobiology of Aging, vol. 17, no. 93, pp. 385–395, 1996.
[37] S. E. Arnold, B. T. Hyman, J. Flory, A. R. Damasio, and G. W. V. Hoesen, “The topographical and neuroanatomical distribution of neu- rofibrillary tangles and neuritic plaques in the cerebral cortex of patients with alzheimer’s disease,” Cerebral Cortex, vol. 1, pp. 103–116, 1991.
[38] D. R. Hinton, A. A. Sadun, J. C. Blanks, and C. A. Miller, “Optic-nerve degeneration in alzheimer’s disease,” New England Journal of Medicine, vol. 315, no. 8, pp. 485–487, 1989.
[39] C. A. Curcio and D. N. Drucker, “Retinal ganglion-cells in alzheimer’s disease and aging,” Annals of Neurology, vol. 33, pp. 248–257, 1993.
12 JOURNAL OF UNDERGRADUATE RESEARCH IN ALBERTA (JURA), VOL. 1, JULY 2011
[40] D.C.Davies,P.McCoubrie,B.Mcdonald,andK.A.Jobst,“Myelinated axon number in the optic-nerve is unaffected by alzheimer’s disease,” British Journal of Ophthalmology, vol. 79, pp. 596–600, 1995.
[41] A. Cronin-Golomb, “Vision in alzheimer’s disease,” Gerontologist, vol. 35, p. 370, 1995.
[42] S. Estermann, G. C. Daepp, K. Cattapan-Ludewig, M. Berkhoff, B. E. Frueh, and D. Goldblum, “Effect of oral donepezil on intraocular pressure in normotensive alzheimer patients,” Journal of Ocular Phar- macology and Therapeutics, vol. 22, pp. 62–67, 2006.
[43] A.Cronin-Golomb,S.Corkin,J.F.Rizzo,andC.J.,“Visualdysfunction in alzheimer’s disease: Relation to normal aging,” Annals of Neurology, vol. 29, pp. 41–52, 1991.
[44] A. Cronin-Golomb, S. Corkin, and J. H. Growdon, “Visual dysfunction predicts cognitive deficits in alzheimer’s disease,” Optometry and Vision Science, vol. 72, pp. 168–176, 1995.
[45] G.C.Cronin-Golomb,A.adGilmore,S.Neargarder,S.R.Morrison,and T. M. Laudate, “Enhanced stimulus strength improvesvisual cognition in aging and alzheimer’s disease,” Cortex, vol. 43, pp. 952–966, 2007.
[46] M. M. Mesulam, “A plasticity-based theory of the pathogenesis of alzheimer’s disease,” Annals of the New York Academy of Sciences, vol. 924, pp. 42–52, 2000.
[47] M. Rizzo, S. W. Anderson, J. Dawson, and M. Nawrot, “Vision and cognition in alzheimer’s disease,” Neuropsychologia, vol. 38, no. 8, pp. 1157–1169, 2000.
[48] C. Bouras, P. R. Hof, P. Giannakopoulos, J. P. Michel, and J. H. Morrison, “Regional distribution of neurofibrillary tangles and senile plaques in the cerebral-cortex of elderly patients – a quantitative- evaluation of a one-year autopsy population from a geriatric hospital,” Cerebral Cortex, vol. 4, pp. 138–150, 1994.
[49] M. A. Westerman, D. Cooper-Blacketer, A. Mariash, L. Kotilinek, T. Kawarabayashi, L. H. Younkin, G. A. Carlson, S. G. Younkin, and K. H. Ashe, “The relationship between abeta and memory in the tg2576 mouse model of alzheimer’s disease,” Journal of Neuroscience, vol. 22, pp. 1858–1867, 2002.
[50] Q. Guo, W. Fu, B. L. Sopher, M. W. Miller, C. B. Ware, G. M. Martin, and M. P. Mattson, “Increased vulnerability of hippocampal neurons to excitotoxic necrosis in presenilin-1 mutant knock-in mice,” Nature Medicine, vol. 5, pp. 101–106, 1999.
[51] N. Gupta and Y. H. Yu ̈cel, “Glaucoma as a neurodegenerative disease,” Current Opinion in Ophthalmology, vol. 18, pp. 110–114, 2007.
[52] S. Oddo, A. Caccamo, M. Kitazawa, B. P. Tseng, and F. M. LaFerla,
“Amyloid deposition precedes tangle formation in a triple transgenic model of alzheimer’s disease,” Neurobiology of Aging, vol. 24, pp. 1063– 1070, 2003.
[53] D. Morgan, D. M. Diamond, P. E. Gottschall, K. E. Ugen, C. Dickey, J. Hardy, K. Duff, P. Jantzen, G. DiCarlo, D. Wilcock, K. Connor, J. Hatcher, C. Hope, M. Gordon, and G. W. Arendash, “A-peptide vaccination prevents memory loss in an animal model of alzheimer’s disease,” Nature, vol. 408, pp. 982–985, 2000.
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