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Functional Implications of Changes in the Senescent Brain: a Review LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES Functional Implications of Changes in the Senescent Brain: A Review CHARLES H.M.BECK SUMMARY: The morphological, chem­ and altered affect. Cholinergic hippo- change, a reduction in ambition and ical, and physiological changes in I he brain campal and neocortical systems were activity, an increased difficulty in accompanying old age are reviewed. The chemically and physiologically abnormal comprehension and an increase in time deterioration of the striatal and hypo­ in the aged. The implications for slowed and effort necessary for performance thalamic dopaminergic systems were im­ cognitive processing and persistance of the of familiar duties. Presenile dementia plicated in the onset of age related memory trace are presented. is viewed as an acceleration of this Parkinsonian-like slowing of performance process of mental deterioration (Kolb, 1968). RESUME: L'auteur passe en revue les emotions modifiee. Les systemes choliner- The first section of this paper changements morphologiques, physiolo- giques de I'hippocampe et du neocortex describes the physically visable, i.e., manifestent aussi chez les vieillards des giques, el chimiques qui accompagnent la morphological changes, that can be vieiles.se. La deterioration des systemes anormalites physiologiques et chimiques. seen in aging brain. Although the dopaminergiques stries et hypothala- L'auteur discute les implications de ces miques est associee chez les vieillards aux changements pour la domaine des pro­ discussion will be restricted to the phenomenes de ralentissement de per­ cessus cognitifs el pour la persistence des literature on normally aging indi­ formance du type Parkinsonien. et aux traces de memoire. viduals and people with presenile and senile dementia, it is noteworthy that a higher than normal incidence of the Dementia refers to a progressive same physical signs have been loss of the mental faculties. The most observed in Down's syndrome common cause of a progressive retardates (Ohara, 1972) and Parkin­ impairment of the mental faculties in son patients (Hirano, 1970). Down's the older adult population is the syndrome retardates develop the degenerative brain disease known as symptoms by age 35 years. In addition senile dementia. If the disease begins to reviewing the physical signs of before the age of 65 years it is referred dementia, the first section of the paper to as presenile dementia or Alzheimer's will discuss the functional implications disease. Presenile and senile dementia of these signs. are diseases of nervous tissue as The second portion of the paper opposed to atherosclerotic dementia describes the chemical and physio­ which is a degenerative disease of the logical correlates of the aging process circulatory system. Together these two and outlines their functional implica­ categories account for the majority of tions. In the third and final section all cases of degenerative brain disease there is a detailed analysis of the in the aged. The incidence of senile behavioral scientist's perspective of dementia is twice as high in women as aging. in men. The proportions are reversed for atherosclerotic dementia (Roth, reported by Kent, 1977). MORPHOLOGICAL SIGNS OF AGING The mental symptoms of senile IN THE BRAIN dementia, from the clinician's Physical evidence for a diagnosis of viewpoint, include flattening of affect, presenile dementia includes the Reprint requests to: Charles Beck. Department of Psychology. Biological Sciences Building. University confusion in spatial and temporal presence in the brain of (I) senile of Alberta, l-dmonton. Alberta. T6G 2E9, Canada. orientation, impairment of memory plaques containing amyloid, an Supported by a grant from the Medical Research especially for recent events, and a immunoglobulin byproduct; (2) Council. general slowing of movements and tangles of neurofibrils, normally Krom the Neuropsychology Unit. Department of though processes. The onset is longitudinally arranged in the nerve Psychology. University of Alberta. Edmonton. Alberta. gradual, beginning with a dislike for fiber and thought to participate in the Vol. 5 No. 4 NOVEMBER 1978-417 Downloaded from https://www.cambridge.org/core. IP address: 170.106.33.19, on 28 Sep 2021 at 20:45:14, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0317167100024203 THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES transport of vital substances along been related to memory impairments Samorajski, 1975). This results in a neurons; (3) areas of degeneration, in humans (Milner, 1970; Victor et al, reduction in oxygen turnover (Chen et consisting of silver staining granules 1971). The memory deficits of the al., 1972). One would predict from this surrounded by spaces or vacuoles; (4) demented and aged have been a reduced cerebral blood flow with age collections of lipofuscin or age attributed to hippocampal damage and with increasing dementia and this pigment inside neurons, representing (Ball, 1977; Malamud, 1972). Other is indeed the case (Lassen et al., I960; an accumulation of oxidized nerve authors (Brizzee et al., 1974; Scheibel Ingvar and Lassen, 1970; Simard, cell membranes; and (5) loss of nerve et al., 1975, 1976) prefer to emphasize 1971). Slowing of cerebral blood flow cells. the importance of the diffuseness of occurs over the temporal region in the It is widely held that the pervasive­ the signs of physical damage brains of memory impaired senile ness of these signs is positively throughout the brain, in accounting patients, and in the parieto-occipito- correlated with the degree of dementia for general slowing of information temporal region in patients with both for patients stricken before age 65 processing accompanying aging. aphasia symptoms (Hagberg and and for those afflicted later in life Prior to the disintegration of the Ingvar, 1976; Obristetal., 1970). Since (Blessed et al., 1968). However, it is nerve cell body there is an age related old people have a greater arterio­ not generally recognized that virtually deterioration of axonal (output) and venous 02 content difference, all people by 80 years of age present dendritic (input) terminal processes indicating the brain is extracting more similar, though less invidious, ex­ (Bondareff and Geinisman, 1976; 02 per unit of blood (Dastur et al., amples of the same physical pathology Machado-Salas et al., 1977; Scheibel 1963), and since the cerebral capillary (Dayan, 1970; Gellerstedt, 1931; et al., 1975, 1976). network of the senescent brain is more Matsuyama et al., 1966). There is a In summary, morphological changes extensive than that of the younger positive correlation between age in the brain with age provide a picture person (Huziker et al., 1978), the related cell loss, severity of tangle of gradual degeneration and cell loss, diminished cerebral blood flow is formation, and degree of granulo- especially in structures involved in more likely a product of metabolic vacuolar degeneration in both memory. The normal aging process is than morphological variables. normals and dements. However, the accelerated in Alzheimer's disease and In presenile and senile dementia, but yearly rate of cell loss is five times as Down's syndrome. Theories of aging not in atherosclerotic dementia, the great in the Alzheimer patients as in emphasize either the relation between occurrence of neurofibrillary tangles is normal persons (Ball, 1977; Ball and hippocampal degeneration and mem­ proportional to the accumulation of Lo, 1977). ory deficits or that between diffuse aluminum in the brain cells (Crapper degeneration and slowed processing. Brody (1955) hypothesized that the et al., 1976). The concentration of The functional implications of neuro- aluminum in Alzheimer patients is degree of dementia is directly related filbrillary tangles and cell membrane to the incidence of cell loss. Meier- four times that in normal patients instability will be detailed in the next (Crapper, 1974; Crapper et al., 1973). Ruge (1975) suggested that this section of the paper. hypothesis is untenable because Implantation of aluminum into the subsequent studies of senescent rodent brains of animals results in neuro­ brains have revealed less than 1% cell CHEMICAL AND PHYSIOLOGICAL fibrillary tangles indentical to those in losses (Brizzee et al., 1968; Klein and SIGNS OF AGING IN THE BRAIN senile humans' brains (Terry and Michel, 1977). However, these studies The most prominent theory of aging Pena, 1965). Aluminum disrupts examined only the rodent neocortex. is the error catastrophe theory of Orgel protein synthesis in nerve cells (Miller Studies of the old rodent's medial (1963; Comfort, 1974). In all tissue, the and Levine, 1974). The origin of the dorsal nucleus of the thalamus (Stein RNA transcription of the genetic code metabolic error causing the aluminum and Firl, 1976) and hippocampus for protein has an increased error rate accumulation is unknown. (Vijayan, 1977) showed serious with age, resulting in the age related Another anabolic process which degeneration. In humans the physical decline in levels of critical enzymes. deteriorates with aging is that of the signs enumerated above appear in Thus there is an age associated decline synthesis, release, and uptake of many parts of the brain including the in uptake, turnover, and utilization of neurotransmitters. Old brains ex­ neocortex. However, the pathology amino acids and a decline in RNA bio­ perience 25% slower rate and 50% has a predilection for the hippo­
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