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Calderwood SK, Murshid A. Molecular Chaperone Accumulation in Cancer and Decrease in Alzheimer's Disease: The Potential Roles of HSF1. Front Neurosci. 2017;11:192doi: 10.3389/fnins.2017.00192.
Calderwood, S. K., & Murshid, A. (2017). Molecular Chaperone Accumulation in Cancer and Decrease in Alzheimer's Disease: The Potential Roles of HSF1. Frontiers in neuroscience, 11192. https://doi.org/10.3389/fnins.2017.00192
Calderwood, Stuart K, and Murshid, Ayesha. "Molecular Chaperone Accumulation in Cancer and Decrease in Alzheimer's Disease: The Potential Roles of HSF1." Frontiers in neuroscience vol. 11 (2017): 192. doi: https://doi.org/10.3389/fnins.2017.00192
Calderwood SK, Murshid A. Molecular Chaperone Accumulation in Cancer and Decrease in Alzheimer's Disease: The Potential Roles of HSF1. Front Neurosci. 2017 Apr 21;11:192. doi: 10.3389/fnins.2017.00192. eCollection 2017. PMID: 28484363; PMCID: PMC5399083.
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Front Neurosci. 2017 Apr 21;11:192. doi: 10.3389/fnins.2017.00192. eCollection 2017.

Molecular Chaperone Accumulation in Cancer and Decrease in Alzheimer's Disease: The Potential Roles of HSF1.

Frontiers in neuroscience

Stuart K Calderwood, Ayesha Murshid

Affiliations

  1. Molecular and Cellular Radiation Oncology, Beth Israel Deaconess Medical Center, Center for Life Sciences 610, Harvard Medical SchoolBoston, MA, USA.

PMID: 28484363 PMCID: PMC5399083 DOI: 10.3389/fnins.2017.00192

Abstract

Molecular chaperones are required to maintain the proteome in a folded and functional state. When challenges to intracellular folding occur, the heat shock response is triggered, leading to increased synthesis of a class of inducible chaperones known as heat shock proteins (HSP). Although HSP synthesis is known to undergo a general decline in most cells with aging, the extent of this process varies quite markedly in some of the diseases associated with advanced age. In Alzheimer's disease (AD), a prevalent protein folding disorder in the brain, the heat shock response of some critical classes of neurons becomes reduced. The resulting decline in HSP expression may be a consequence of the general enfeeblement of many aspects of cell physiology with aging and/or a response to the pathological changes in metabolism observed specifically in AD. Cancer cells, in contrast to normal aging cells, undergo

Keywords: Alzheimer's disease; cancer; heat shock protein; molecular chaperone; proteotoxic stress

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