ExperimentalGerontology,Vol.26, pp. 615-621, 1991 Printedin the USA.All rightsreserved.
0531-5565/91$3.00 + .00 Copyright©1991PergamonPressplc
BOOK REVIEWS
Psychoneuroendocrinology of Aging: Basic and Clinical Aspects. Fida Research Series, Vol. 16, by G. Valenti (Ed.), Springer-Verlag, New York, 1988, ISBN 0-387°96943-8, 179 pp. Tins VOLt~_Econtains the proceedings of the Satellite Workshop of the XIX Congress of the Italian Society of Psychoneuroendocrinology, held in Parma, Italy, 29-30 August, 1988. The theme was to present the latest findings about the hypothalamo-pituitary-endocrine axis; discuss changes in these neuroendocrine relationships with age; evaluate these findings as a basis for a new pathogenetic theory of aging; and develop new biomarkers for the diagnosis, treatment, and follow-up of the aging brain. The conference focused on three aspects of the psychoneuroendocrine pattern in aging. Part I examined hormono-metabolic changes with physiological aging; Part II was concerned with changes with pathological aging--i.e., the changes which occur in Alzheimer's disease, multi-infarct dementia, Parkinson's disease, and depression; and Part III briefly speculated about future patterns for research in this field. Part I included chapters entitled "Changes in Membrane and Calcium Mediated Signals in Senescence," "Hypothalamic Regulation of Pituitary-Gonadal function," "Psychoneuroendocrine Control of Pituitary TSH secretion and Aging," "The Hypothalamic-SomatotrophSomatomedin Axis and Aging," "Defective Growth Hormone Secetion in Aging Mammals," "The Hypothalamic-Pitultary Adrenal Axis in Aging," "Physiological Aging Brain and Psychoneuroendocrine Control of ADH Secretion," and "The Effect of Testosterone Replacement on Growth Hormone Secretion in Aged Rats." Part II discussed neuroendocrine changes in a number of age-related diseases. The conclusion was that (1) the spectrum of normal aging-related hormonal changes was very large and was not unlike the nonspecific and nondiagnostic changes which are frequently seen in age-related diseases; (2) aging and age-related diseases may thus represent a continuum of alterations related to impairments of the same cerebral processes; and (3) aging should therefore not be considered just a natural event, but rather a pathological situation deserving specific brain analysis and treatments. Part III reviewed cellular and molecular aspects of the psychoneuroendocrinimmunology of aging, summarizing the interrelationships between the aging neuroendocrine system and aging-related immunological changes. Clearly, a great deal of material is presented in this little volume. The concise chapters are not just reviews of the literature but are also reports of ongoing research. Few words are wasted, and the chapters are uniformly well-referenced. Nevertheless, there are some major omissions. Chief among them is the total neglect of the pineal gland and its hormones. The 1 skimpy index, just over 2 ~ pages, could easily have been expanded. The typography varies from chapter to chapter, indicating that the book was published from individually submitted camera-ready copy. Unfortunately, this contributed to a greater-than-normal number of typographical errors, which detracted from the readability. On the other hand, this direct-publica615
616
BOOKREVIEWS
tion technique reduced the time lag from presentation to publication, thereby increasing the timeliness of the book. This book should be acquired by clinicians and scientists in the fields of endocrinology, neuroscience, and immunology. WARD DEAN The Center for Bio-Gerontology Pensacola, FL
Regulation of Neuroendocrine Aging. Vol. 24. Interdisciplinary Topics in Gerontology, by A.V. Everitt and J.R. Walton (Eds.), H.P. yon Hahn (Series Ed.), Karger, Basel, Switzerland, 1988, ISBN 3-8055-4770-6, 155 pp. This is the latest in Karger's hallmark gerontological series and upholds the high standards of previous volumes. The underlying thesis of the book (with a few exceptions) is that aging is either due primarily to, or influenced by, a progressive loss of neuroendocrine homeostasis, mediated by loss of hypothalamic sensitivity to negative feedback inhibition. In the first of two chapters authored by the senior editor, the relationships between the central and peripheral endocrine glands are briefly reviewed. The tone and underlying thesis of the book are presented--that aging phenomena are regulated by the hypothalamo-pituitary axis and that with greater understanding of the functioning of this system, rejuvenation techniques will be applicable to humans in the forseeable future. The editors also reviewed agerelated changes in the hypothalamo-pituitary-endocrine axis in greater detail. In another chapter, the senior editor discussed various aspects of the antiaging action of hypophysectomy. Paul Segall and Hal Sternberg review several possible mechanisms to which the loss of hypothalamic control with age may be attributed. These include (1) accumulated damage from oxidative free radicals, (2) loss of brain cells due to the toxic effects of high levels of certain steroid hormones, and (3) programmed cell death. These theories are examined in light of the known life-extending effects of caloric and tryptophan restriction. They suggest that the mechanism of these regimens in extending lifespan may be due to either reduced levels of steroid hormone production or to reduced rates of cell loss. Finally, they propose that understanding reproductive senescence in the female rodent model may provide the best means of understanding the aging process itself. Joseph Meites discusses the neuroendocrine basis of aging in the rat. He defines aging in terms of decreased function of organs and tissues, associated with a reduced ability to maintain homeostasis. He believes the three important aging events in the life of the rat include (1) a decline in reproductive function, (2) development of mammary and pituitary tumors, and (3) decreased growth hormone and somatomedin secretion and protein synthesis. Furthermore, he believes that age-related hypothalamic dysfunctions are primarily responsible for these changes. Various causes of damage to the hypothalamus are suggested, including neuronal loss due to toxic actions of various hormones, and accumulation of free radicals, cross-linkages, and "cellular debris" like lipofuscin. Finally, he shows that correction of hypothalamic deficiencies can alleviate or ameliorate the deleterious changes that take place