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Dennis J. Selkoe, MD

Arch Neurol. 2005;62:192-195.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

An explosion of new techniques to explore DNA and protein biology during the last 2 decades has illuminated one of the most enigmatic and intractable subjects in biomedicine—neurodegeneration. Eponymic diseases of the nervous system that were until recently characterized by mechanistic ignorance and therapeutic nihilism are falling steadily to the power of molecular genetics, cell biology, biochemistry, and animal modeling. Alzheimer, Huntington, Creutzfeld-Jacob, and Parkinson diseases, as well as amyotrophic lateral sclerosis, spinocerebellar atrophies, frontotemporal dementia, and other previously obscure diseases, have all yielded rapid progress in the deciphering of their biochemical pathology and genetic underpinnings. This sea change in our understanding of a group of incurable diseases that confer enormous personal and societal burdens has brought us to the verge of rationally designed therapies and, in some cases, into actual human trials.

Perhaps the foremost example, both in terms of its impact on society and . . . [Full Text of this Article]

A WELL-DEFINED NEUROPATHOLOGY SPURRED THE QUEST FOR THERAPY

GENETIC DEFECTS THAT PREDISPOSE TO AD STRONGLY IMPLICATE A

TAU MUTATIONS LEAD TO FRONTOTEMPORAL DEMENTIA AND RELATED DISORDERS WITHOUT INDUCING A DEPOSITION

ELUCIDATION OF THE PATHOGENIC PATHWAY PROVIDES MOLECULAR TARGETS AMENABLE TO BIOTECHNOLOGY

WHERE DO WE GO FROM HERE?

AUTHOR INFORMATION

Author Affiliations: Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass.

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