Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21

Endriyas Kelta Wabalo; Chala Kenenisa Edae

doi:doi:10.11648/j.cb.20180602.12

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Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21

Endriyas Kelta Wabalo, Chala Kenenisa Edae

Published in Cell Biology (Volume 6, Issue 2)

Received: 9 November 2018 Accepted: 19 December 2018 Published: 4 January 2019

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Abstract

The presence of “plaques” and “tangles” in the brain is considered as the hallmark of Alzheimer’s disease. The major constituent of the plaques is a protein (“A-beta”) which is split off from a much larger parent protein called Amyloid Precursor Protein (APP), and that of tangles is the protein tau, which normally functions to stabilize microtubules within neuronal axons. There are several possibilities that elaborate the change in amyloid formation and its consequences on the neuronal death to bring AD; the first is the amyloid cascade hypothesis that describes how early-onset AD is induced by mutations in APP, the presenilins and apoE4. The second possibility is the calcium hypothesis of Alzheimer’s disease, which argues the calcium-induced memory loss in Alzheimer’s disease. Mapping of the gene that encodes the precursor protein (APP) of the β-amyloid (Aβ) present in the Aβ plaques in both AD and DS to chromosome 21 was strong evidence that the chromosome 21 gene product was a principal neuropathogenic culprit in the AD as well as DS. The main objective of this review was elucidate the possible hypothesis of Alzheimer’s disease and to pinpoint the chromosome 21 gene product as principal neuropathogenic culprit in the pathogenesis of AD and DS. Different articles on pathogenesis of AD and its link to DS were revised. As conclusion, different hypothesis on AD pathogenesis discussed on this review illustrated well about the pathogenesis of AD, its link to DS and potential target for certain therapeutic agents to act on the treatment of AD and DS.

Published in	Cell Biology (Volume 6, Issue 2)
DOI	10.11648/j.cb.20180602.12
Page(s)	33-46
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2019. Published by Science Publishing Group

Keywords

Alzheimer’s Disease, Trisomy 21, Amloid Protein, Amloid Protien Plaques, Ameloid Protein Tangles

References

[1]	Alzheimer Society of Canada (2010). Down syndrome and Alzheimer’s disease. pp. 1-8.
[2]	Alzheimer’s Association (2012). Down syndrome and Alzheimer’s disease. A topic in the Alzheimer’s Association series on understanding dementia; pp. 1-4.
[3]	Alzheimer’s Australia (2012). Down syndrome and Alzheimer’s disease. Help sheet; pp. 1-2.
[4]	Berridge M. J. (2014). Signalling Defects and Disease. Cell Signalling Biology; doi: 10.1042/csb0001012.
[5]	Conti E., Galimberti G., Piazza F., Raggi E. M., and Ferrarese C. (2010). Increased sAPPα, Abeta 1-42, and Anti-Abeta 1-42 Antibodies in Plasma from Down syndrome Patients. www.alzheimerjournal.com. Alzheimer Dis Assoc Disord; 24( 1):96-100.
[6]	Wilcock M. D. and Griffin T. W. (2013). Down’s syndrome, neuroinflammation, and Alzheimer neuropathogenesis. Journal of Neuroinflammation; 10(84): 1-10.
[7]	Anckar J. and Sistonen L. (2011). Regulation of HSF1 Function in the Heat Stress Response: Implications in Aging and Disease. Annu. Rev. Biochem.; 80:1089–115.
[8]	Coppus W. M., Schuur M., Vergeer J., Janssens W. J., Oostra A. B., Verbeek M. M. and van Duijn M. C. (2012). Plasma amyloid and the risk of Alzheimer’s disease in Down syndrome. Neurobiology of Aging; 33: 1988–1994.
[9]	Head E., PowellD., GoldT. B., and SchmittA. F. (2012). Alzheimer's disease in Down’s syndrome. Eur J Neurodegener Dis.; 1(3): 353–364.
[10]	Moran J., Hogan M., Srsic-Stoehr K., and Rowlett S. (2013). Aging and Downs Syndrome: A Health & Well-Being Guidebook. National Down’s syndrome Society; pp. 1-44.
[11]	Rafii S. M. (2014). Pro: Are we ready to translate Alzheimer's disease modifying therapies to people with Down syndrome? Alzheimer's Research & Therapy; 6 (60): 1-4.
[12]	Down syndrome and Alzheimer’s disease (2018). Review on Dementia Australia help sheet dementia.org.au.P1-5.
[13]	Dekker, A. D., Vermeiren, Y., Carmona-Iragui, M., Benejam, B., Videla, L., De Deyn, P. P. (2018). Monoaminergic impairment in Down syndrome with Alzheimer's disease compared to early-onset Alzheimer's disease. Alzheimer's and dementia (Amsterdam, Netherlands), 10, 99-111. DOI: 10.1016/j.dadm.2017.11.001
[14]	Cheon M. S., Fountoulakis M., Cairns N. J., Dierssen M.., Herkner K., and Lubec G. (2018). Decreased protein levels of stathmin in adult brains with Down syndrome and Alzheimer's disease. Protein Expression in Down syndrome Brain © Springer-Verlag/Wien.p 281-282.
[15]	Pogacar S. and Rubio A. (2010). Morphological Features of Pick’s and Atypical Alzhcimer’s Disease in Down’s syndrome. Acta Neuropathol (Hen), 58:249-254.

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APA Style

Endriyas Kelta Wabalo, Chala Kenenisa Edae. (2019). Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21. Cell Biology, 6(2), 33-46. https://doi.org/10.11648/j.cb.20180602.12

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ACS Style

Endriyas Kelta Wabalo; Chala Kenenisa Edae. Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21. Cell Biol. 2019, 6(2), 33-46. doi: 10.11648/j.cb.20180602.12

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AMA Style

Endriyas Kelta Wabalo, Chala Kenenisa Edae. Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21. Cell Biol. 2019;6(2):33-46. doi: 10.11648/j.cb.20180602.12

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@article{10.11648/j.cb.20180602.12,
  author = {Endriyas Kelta Wabalo and Chala Kenenisa Edae},
  title = {Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21},
  journal = {Cell Biology},
  volume = {6},
  number = {2},
  pages = {33-46},
  doi = {10.11648/j.cb.20180602.12},
  url = {https://doi.org/10.11648/j.cb.20180602.12},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20180602.12},
  abstract = {The presence of “plaques” and “tangles” in the brain is considered as the hallmark of Alzheimer’s disease. The major constituent of the plaques is a protein (“A-beta”) which is split off from a much larger parent protein called Amyloid Precursor Protein (APP), and that of tangles is the protein tau, which normally functions to stabilize microtubules within neuronal axons. There are several possibilities that elaborate the change in amyloid formation and its consequences on the neuronal death to bring AD; the first is the amyloid cascade hypothesis that describes how early-onset AD is induced by mutations in APP, the presenilins and apoE4. The second possibility is the calcium hypothesis of Alzheimer’s disease, which argues the calcium-induced memory loss in Alzheimer’s disease. Mapping of the gene that encodes the precursor protein (APP) of the β-amyloid (Aβ) present in the Aβ plaques in both AD and DS to chromosome 21 was strong evidence that the chromosome 21 gene product was a principal neuropathogenic culprit in the AD as well as DS. The main objective of this review was elucidate the possible hypothesis of Alzheimer’s disease and to pinpoint the chromosome 21 gene product as principal neuropathogenic culprit in the pathogenesis of AD and DS. Different articles on pathogenesis of AD and its link to DS were revised. As conclusion, different hypothesis on AD pathogenesis discussed on this review illustrated well about the pathogenesis of AD, its link to DS and potential target for certain therapeutic agents to act on the treatment of AD and DS.},
 year = {2019}
}

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TY  - JOUR
T1  - Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21
AU  - Endriyas Kelta Wabalo
AU  - Chala Kenenisa Edae
Y1  - 2019/01/04
PY  - 2019
N1  - https://doi.org/10.11648/j.cb.20180602.12
DO  - 10.11648/j.cb.20180602.12
T2  - Cell Biology
JF  - Cell Biology
JO  - Cell Biology
SP  - 33
EP  - 46
PB  - Science Publishing Group
SN  - 2330-0183
UR  - https://doi.org/10.11648/j.cb.20180602.12
AB  - The presence of “plaques” and “tangles” in the brain is considered as the hallmark of Alzheimer’s disease. The major constituent of the plaques is a protein (“A-beta”) which is split off from a much larger parent protein called Amyloid Precursor Protein (APP), and that of tangles is the protein tau, which normally functions to stabilize microtubules within neuronal axons. There are several possibilities that elaborate the change in amyloid formation and its consequences on the neuronal death to bring AD; the first is the amyloid cascade hypothesis that describes how early-onset AD is induced by mutations in APP, the presenilins and apoE4. The second possibility is the calcium hypothesis of Alzheimer’s disease, which argues the calcium-induced memory loss in Alzheimer’s disease. Mapping of the gene that encodes the precursor protein (APP) of the β-amyloid (Aβ) present in the Aβ plaques in both AD and DS to chromosome 21 was strong evidence that the chromosome 21 gene product was a principal neuropathogenic culprit in the AD as well as DS. The main objective of this review was elucidate the possible hypothesis of Alzheimer’s disease and to pinpoint the chromosome 21 gene product as principal neuropathogenic culprit in the pathogenesis of AD and DS. Different articles on pathogenesis of AD and its link to DS were revised. As conclusion, different hypothesis on AD pathogenesis discussed on this review illustrated well about the pathogenesis of AD, its link to DS and potential target for certain therapeutic agents to act on the treatment of AD and DS.
VL  - 6
IS  - 2
ER  -

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Author Information

Endriyas Kelta Wabalo

Biomedical Sciences, Institute of Health, Jimma University, Jimma, Ethiopia
Chala Kenenisa Edae

Biomedical Sciences, Institute of Health, Jimma University, Jimma, Ethiopia

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APA Style

Endriyas Kelta Wabalo, Chala Kenenisa Edae. (2019). Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21. Cell Biology, 6(2), 33-46. https://doi.org/10.11648/j.cb.20180602.12

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ACS Style

Endriyas Kelta Wabalo; Chala Kenenisa Edae. Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21. Cell Biol. 2019, 6(2), 33-46. doi: 10.11648/j.cb.20180602.12

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AMA Style

Endriyas Kelta Wabalo, Chala Kenenisa Edae. Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21. Cell Biol. 2019;6(2):33-46. doi: 10.11648/j.cb.20180602.12

Copy | Download

@article{10.11648/j.cb.20180602.12,
  author = {Endriyas Kelta Wabalo and Chala Kenenisa Edae},
  title = {Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21},
  journal = {Cell Biology},
  volume = {6},
  number = {2},
  pages = {33-46},
  doi = {10.11648/j.cb.20180602.12},
  url = {https://doi.org/10.11648/j.cb.20180602.12},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20180602.12},
  abstract = {The presence of “plaques” and “tangles” in the brain is considered as the hallmark of Alzheimer’s disease. The major constituent of the plaques is a protein (“A-beta”) which is split off from a much larger parent protein called Amyloid Precursor Protein (APP), and that of tangles is the protein tau, which normally functions to stabilize microtubules within neuronal axons. There are several possibilities that elaborate the change in amyloid formation and its consequences on the neuronal death to bring AD; the first is the amyloid cascade hypothesis that describes how early-onset AD is induced by mutations in APP, the presenilins and apoE4. The second possibility is the calcium hypothesis of Alzheimer’s disease, which argues the calcium-induced memory loss in Alzheimer’s disease. Mapping of the gene that encodes the precursor protein (APP) of the β-amyloid (Aβ) present in the Aβ plaques in both AD and DS to chromosome 21 was strong evidence that the chromosome 21 gene product was a principal neuropathogenic culprit in the AD as well as DS. The main objective of this review was elucidate the possible hypothesis of Alzheimer’s disease and to pinpoint the chromosome 21 gene product as principal neuropathogenic culprit in the pathogenesis of AD and DS. Different articles on pathogenesis of AD and its link to DS were revised. As conclusion, different hypothesis on AD pathogenesis discussed on this review illustrated well about the pathogenesis of AD, its link to DS and potential target for certain therapeutic agents to act on the treatment of AD and DS.},
 year = {2019}
}

Copy | Download

TY  - JOUR
T1  - Possible Hypothesis on Alzheimer’s Disease Pathogenesis and Its Link to Trisomy 21
AU  - Endriyas Kelta Wabalo
AU  - Chala Kenenisa Edae
Y1  - 2019/01/04
PY  - 2019
N1  - https://doi.org/10.11648/j.cb.20180602.12
DO  - 10.11648/j.cb.20180602.12
T2  - Cell Biology
JF  - Cell Biology
JO  - Cell Biology
SP  - 33
EP  - 46
PB  - Science Publishing Group
SN  - 2330-0183
UR  - https://doi.org/10.11648/j.cb.20180602.12
AB  - The presence of “plaques” and “tangles” in the brain is considered as the hallmark of Alzheimer’s disease. The major constituent of the plaques is a protein (“A-beta”) which is split off from a much larger parent protein called Amyloid Precursor Protein (APP), and that of tangles is the protein tau, which normally functions to stabilize microtubules within neuronal axons. There are several possibilities that elaborate the change in amyloid formation and its consequences on the neuronal death to bring AD; the first is the amyloid cascade hypothesis that describes how early-onset AD is induced by mutations in APP, the presenilins and apoE4. The second possibility is the calcium hypothesis of Alzheimer’s disease, which argues the calcium-induced memory loss in Alzheimer’s disease. Mapping of the gene that encodes the precursor protein (APP) of the β-amyloid (Aβ) present in the Aβ plaques in both AD and DS to chromosome 21 was strong evidence that the chromosome 21 gene product was a principal neuropathogenic culprit in the AD as well as DS. The main objective of this review was elucidate the possible hypothesis of Alzheimer’s disease and to pinpoint the chromosome 21 gene product as principal neuropathogenic culprit in the pathogenesis of AD and DS. Different articles on pathogenesis of AD and its link to DS were revised. As conclusion, different hypothesis on AD pathogenesis discussed on this review illustrated well about the pathogenesis of AD, its link to DS and potential target for certain therapeutic agents to act on the treatment of AD and DS.
VL  - 6
IS  - 2
ER  -

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