Front Temporal Dementia

Paper Summary:

This paper discusses the literature on the topic of front temporal dementia to see what has been investigated to date and what results have been found, as well as suggestions for future research and for new areas to explore, in order to refine the issue further and to gain more insight into causes, diagnosis, and treatments that might be effective. The paper examines the many aspects of FTD and points out the differences in onset and also in treatment. The writer believes that the discovery of the connection to mutations in the tau gene has opened up a wide variety of possibilities for further study, but notes that there are FTD subtypes that certainly do not have a link with the tau gene and may have a different cause and may also have to be treated differently.

Outline:
Introduction
Prevalence
Diagnosis
Chemical Processes
Therapy
Conclusion

From the Paper:

"Front temporal dementia (FTD) takes place in those parts of the brain preferentially affected by the problem of dementia, which is itself caused by differing pathological processes leading to damage in the frontal and/or the temporal parts of the brain. These areas are largely responsible for such clinical manifestations as behavior, emotional response, and language skills. Damage in these areas can give rise to forms of frontal dementia and language disorders such as semantic dementia and primary progressive aphasia. This damage is linked to dysfunctions of the tau gene or tau protein and can lead to a classification based on specific clinical symptoms or particular lesions or even a mixed classification."

Sample of Sources Used:

• Allain, Herve, Daniele Bentue-Ferrer, Olivier Tribut, Marc Me'rienne, and Serge Belliard. "Drug therapy of frontotemporal dementia." Human Psychopharmacoly Clin Exp (2003), 221-225.
• Baker, Matt, Ian R. Mackenzie, Stuart M. Pickering-Brown, Jennifer Gass, Rosa Rademakers, Caroline Lindholm, Julie Snowden, Jennifer Adamson, A. Dessa Sadovnick, Sara Rollinson, Ashley Cannon, Emily Dwosh, David Neary, Stacey Melquist, Anna Richardson, Dennis Dickson, Zdenek Berger, Jason Eriksen, Todd Robinson, Cynthia Zehr, Chad A. Dickey, Richard Crook, Eileen McGowan, David Mann, Bradley Boeve, Howard Feldman, and Mike Hutton. "Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17." Nature, Vol 442, number 24 (August 2006), 1038
• Bird, Thomas D., David Nochlin, Parvoneh Poorkaj, Monique Cherrier, Jeffrey Kaye, Haydeh Payami, Elaine Peskind, Thomas H. Lampe, Ellen Nemens, Philip J. Boyer, and Gerard D. Schellenberg1. "A clinical pathological comparison of three families with frontotemporal dementia and identical mutations in the tau gene." Brain, 122 (1999), 741-756
• Buee, Luc, Thierry Bussiere, Valerie Buee-Scherrer, Andre Delacourte, and Patrick R. Hof. Brain Research Reviews 33 (2000), 95-130.
• Cruts, Marc, Ilse Gijselinck, Julie van der Zee1, Sebastiaan Engelborghs, Hans Wils, Daniel Pirici, Rosa Rademakers, Rik Vandenberghe, Bart Dermaut, Jean-Jacques Martin, Cornelia van Duijn, Karin Peeters, Raf Sciot, Patrick Santens, Tim De Pooter, Maria Mattheijssens, Marleen Van den Broeck, Ivy Cuijt, Krist'l Vennekens, Peter P. De Deyn, Samir Kumar-Singh, and Christine Van Broeckhoven1. "Null mutations in progranulin cause ubiquitinpositive frontotemporal dementia linked to chromosome 17q21." Nature, Volume 224, Number 24 (August 2006), 1038.

More papers on Front Temporal Dementia:

• Descriptive Essay # 131308 : "Front Temporal Dementia"
• Analytical Essay # 142817 : "Pathophysiology of Age-Associated Dementia"
• Term Paper # 120665 : "Vascular Dementia"

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