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Nadine Joseph
Annotated Bibliography
1.
Agorogiannis EI, Agorogiannis GI, Papadimitriou A, Hadjigeorgiou GM.
Protein misfolding in neurodegenerative diseases. Neuropathol Appl
Neurobiol 2004;30(3):215-24.
As indicated in the title, the paper makes the correlation between protein misfolding and
neurodegenerative diseases, such as AD, PD, and Huntington’s disease, among others. In
this review, they explain the steps of how a misfolded proteins cause certain pathologies.
They describe in detail the protein misfolding mechanisms in AD, PD, and Huntington’s
disease. Lastly, they briefly discuss chaperones and their involvement with misfolded
proteins.
2.
Craft JM, Watterson DM, Van Eldik LJ. Human amyloid beta-induced
neuroinflammation is an early event in neurodegeneration. Glia
2006;53(5):484-90.
This paper develops the connection between neuroinflammation and neurodegenerative
disorders, in particular AD. Though the paper is not strong in method nor conclusion, the
paper does give a brief overview of the neuroinflammatory factors upregulated in the
early stages of neurodegeneration.
3.
Hoozemans JJ, Veerhuis R, Rozemuller JM, Eikelenboom P.
Neuroinflammation and regeneration in the early stages of Alzheimer's
disease pathology. Int J Dev Neurosci 2005.
This review paper is similar to the previous paper. In addition to outlining the
neuroinflammatory response in AD, it explains the role of Cox-2, microglia activation in
the pathology of AD. The paper also includes a pathological cascade for AD,
incorporating Cox-2, neuroinflammation, neuroregeneration.
4.
Macario AJ, Conway de Macario E. Sick chaperones, cellular stress, and
disease. N Engl J Med 2005;353(14):1489-501.
This paper is an excellent review on chaperones and cellular stress. The paper is
particularly helpful by including a list of cellular stressor as well as a diagram of the life
phase of a protein. The article ends with a discussion of chaperones and the pathologies
associated with them.
5.
Mattson MP. Pathways towards and away from Alzheimer's disease.
Nature 2004;430(7000):631-9.
This paper is an excellent review on AD. The paper provides a thorough background on
AD, including its symptoms, pathology, biochemical and genetic origins, as well as a
brief discussion of therapeutics.
6.
Oddo S, Caccamo A, Shepherd JD, Murphy MP, Golde TE, Kayed R,
Metherate R, Mattson MP, Akbari Y, LaFerla FM. Triple-transgenic model
of Alzheimer's disease with plaques and tangles: intracellular Abeta and
synaptic dysfunction. Neuron 2003;39(3):409-21.
This paper introduces a novel animal model for AD. In the paper, the model is verified
through a series of assays. This paper is particularly relevant for those looking for an
animal model that exhibits all the molecular characteristics of AD.
7.
Ross CA, Poirier MA. Protein aggregation and neurodegenerative
disease. Nat Med 2004;10 Suppl:S10-7.
This review describes the link between protein aggregation and neurodegenerative
diseases. The paper briefly describes the mechanism of protein aggregation in several
neurodegenerative diseases. This description includes a flowchart of a theoretical multistep pathway for protein aggregation. The paper ends with a discussion of possible
therapeutic strategies.
8.
Ross CA, Poirier MA. Opinion: What is the role of protein aggregation in
neurodegeneration? Nat Rev Mol Cell Biol 2005;6(11):891-8.
This paper is very similar to the previous review by Ross and Poirier. In essence, this
paper is a recapitulation of the first review.
9.
Selkoe DJ. Cell biology of protein misfolding: the examples of Alzheimer's
and Parkinson's diseases. Nat Cell Biol 2004;6(11):1054-61.
This review provides a thorough explanation of the corollary between misfolded proteins
and the pathologies found in neurodegenerative diseases. The paper describes the
mechanisms of protein misfolding using AD and PD as their primary examples. Of both
examples, the paper more heavily focuses on AD. In addition, the paper raises interesting
connections between the two diseases.
10.
Smith RC, Rosen KM, Pola R, Magrane J. Stress proteins in Alzheimer's
disease. Int J Hyperthermia 2005;21(5):421-31.
This review paper provides a good discussion of the stress proteins involved in AD. In
particular, the paper describes the role of Hsp 70 in reversing the cytotoxic effects of Aβ
accumulation. Secondly, the paper illuminates the connection of Hsp 70/Hsp 90 with the
removal of hyperphosphorylated tau. This paper is crucial for developing one’s
knowledge of the stress response in AD.