The concepts of aging-related cognitive changes and dementia have appeared in philosophical and scientific writings since ancient times. Starting in 7th century b.c. Greece, many intellectuals from Pythagoras to Galen weighed in with various opinions on the matter, but few suggested causes beyond speculations. Hippocrates, for example, thought that "paranoia," or aging-related mental decline, was caused by cooling and drying of the brain and was fatal (Berchtold and Cotman, 1998). In the latter part of the 17th century, a resurgence of interest in cadaveric dissection led to the examination of brains from elderly individuals in an attempt to understand changes related to aging. For instance, the English pathologist Matthew Baillie became the first to address the concept of brain atrophy with aging and dementia when he noted ventricular enlargement in the brains of some demented individuals. In the early 19th century, the conceptualization and treatment of the mentally ill were revolutionized by the work of the French physician Phillippe Pinel. Drawing on the writings of Galen, Cullen, and others in his work A Treatise on Insanity, Pinel (1806) suggested that mental illness was a disease that could be the subject of empirical study. Pinel also championed

Textbook of Biological Psychiatry. Edited by Jaak Panksepp Copyright © 2004 by Wiley-Liss, Inc. ISBN: 0-471-43478-7

more humanitarian treatment of the mentally ill. He was the first to use the term senile dementia (leading to the use of the term senility as a medical diagnosis) and wrote that this was an inevitable part of aging. Pinel's student Pierre Esquirol differentiated developmental amentia, or idiocy, from dementia, which he thought resulted from disease. He also suggested several causes of dementia, including aging, and noted that multiple forms of psychopathology could be seen in demented individuals (Berchtold and Cotman, 1998).

In the late 19th century, advances in neuroscience gave rise to new understandings of the brain and of dementia. Morel (1860) and Wilks (1865) correlated a decrease in brain weight and an increase in sulcal size, respectively, with aging and cognitive decline. The revelation that neurosyphilis is associated with a decrease in vascular caliber in the brain preceded the seminal work of Alzheimer and Binswanger in the 1890s, which associated arteriosclerotic disease with brain atrophy and dementia (Roman, 1999). In 1892 Blocq and Marinesco first described cerebral plaques, and by 1907 Fischer wrote that plaques were a hallmark of dementia (Berchtold and Cot-man, 1998). Simchowicz (1911) was the first to use the term senile plaque and held that plaque quantity correlated with disease severity. Following on Bielschowsky's description of neurofibrils, Alzheimer (1907) described his classic case (see below) and was the first to describe neurofibrillary tangles associated with neuronal degeneration. Given the relatively young age of his patient and the widespread tangles he noted, Alzheimer hypothesized that his patient had a previously undescribed disease that was distinct from senile dementia.

In Textbook of Psychiatry, Emil Kraepelin (1910) recognized and codified the use of the term Alzheimer's disease (AD). Kraepelin stopped short of stating that AD was distinct from senile dementia, though, and mentioned the possibility that it simply represented precocious senility. In discussing dementia in general, Kraepelin recognized its association with memory loss, language changes, personality changes, delusions, and depression as well as other forms of cognitive impairment and psychopathology.

In the mid-20th century, neuropathological studies led to increased confusion about the relationships between normal aging, AD, and senile dementia. Following on the work of Grunthal, Gellerstedt found that most normal elderly individuals had some brain plaques and tangles (Berchtold and Cotman, 1998). The nature of plaques was debated until the 1960s when electron microscopy showed plaques to be composed of an amyloid core with surrounding cellular elements, and tangles were shown to be composed of abnormal neurofilaments. In addition, clinical and neuropathological evidence suggested that AD was not distinct from senile dementia, and the two concepts were later unified (Halpert, 1983). The work of Blessed and colleagues (1968) clarified clinical criteria used to diagnose AD and showed a correlation between disease burden and illness.

Building on the work of these pioneers, modern investigators are intensively studying the cognitive and psychological changes associated with normal aging as well as AD and other causes of dementia. Numerous advances have been made in recent years in the nosology, epidemiology, genetics, clinical characteristics, and neuroanatomi-cal and neurochemical changes of dementing illnesses, and these advances have led to increased diagnostic sophistication and new treatment approaches. The therapeutic nihilism that has dominated scientific and popular thought since the time of Hippocrates is today giving way to new hope for dementia sufferers and their families.

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