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The Effect of Aging on People with Brain Injuries Since aging produces a number of neurological problems in and of itself, such as senile dementia, it is important to discover what may happen to people with brain injury as they get older. Certain biochemical studies have shown that people with brain injuries may produce the protein that is found in the brains of people with Alzheimer's Disease. There could be a link between suffering a brain injury while one is young, and developing Alzheimer's Disease later in life. As America's senior citizen population grows, the number of senior citizens will likewise grow. The aging of the population with brain injuries has not been examined extensively. Before 1980, the majority of people with signifigant brain injuries were "dead on arrival." Therefore, until the last two decades, the population available for observation was vanishingly small. In the last ten years, there have been a number of studies on a possible relation between previous brain injury and Alzheimer's Disease. A handful of studies have examined other possible neurological effects of aging on people with brain injuries. The relationship between Alzheimer's Disease and previous brain injury is, at best, ambiguous. Studies have see-sawed over linking the two or separating them. The most recent study to advocate separating them is the 1999 Rotterdam study of over six thousand individuals, which found no link between Alzheimer's Disease and previous traumatic brain injury or Alzheimer's Disease and a gene called APO-e4. This study, however, looked only at people with mild traumatic brain injuries, and not at those with severe or moderate injuries. Studies linking Alzheimer's Disease and previous brain injury are not uniform in defining what the relationship may be. The 1995 article by Mayeux et al. in Neurology looked at about two hundred people, of whom about half had Alzheimer's Disease, and about ten percent of that two hundred were people with brain injuries. The study showed that people with the APO-e4 gene were more likely to develop Alzheimer's Disease than the rest of the population, and that people with brain injuries who also had the APO-e4 gene were still more likely to develop Alzheimer's Disease. A link between previous brain injuries and the development of Alzheimer's Disease without the presence of the APO-e4 gene was not seen. The contemporaneous article by Rasmusson et al. in Brain Injury was a comparison of reports of brain injury by the spouses of people with Alzheimer's Disease and the spouses of normal people. It used sixty-eight couples. The authors claim to have demonstrated a link between "sporadic" Alzheimer's Disease (cases of Alzheimer's Disease that happen in people without a family history of Alzheimer's Disease) and a previous brain injury. However, this is the smallest sample of any of the studies. According to statisticians, a sample size between one hundred and fifty and two hundred is the lower limit for a group study. Salib and Hillier's joint article in the International Journal of Geriatric Psychiatry studied a total of five hundred and thirty-eight people, split between people with sporadic Alzheimer's Disease, familial Alzheimer's Disease, and people without Alzheimer's Disease. Although they claimed to find a link between previous brain injury and Alzheimer's Disease, they did not check for any link to the APO-e4 gene. Also, they claimed to find a link between previous brain injury and other degenerative disorders of the nervous system, such as vascular dementia. The 1998 Kerr and Krause article in AACN Clinical Issues is an overview of research done up until that date. The authors state that the presence of the APO-e4 gene creates problems in recovery after brain injury and other neurological insults, like stroke, creating the tangles and plaques seen in Alzheimer's Disease. This assertion is backed by research on brain injury complications and that gene done by Graham et al., reported in their 1999 article in Acta Neurochirurgica Supplementum and Jordan et al., reported in the July 9, 1997 issue of the Journal of the American Medical Association. Apparently, one of the problems is that the APO-e4 gene makes a weaker cellular structure, that, in long, thin cells like most nerve cells, makes them too limp and tends to get them tangled. The 1999 Yamada et al. article in the Journal of the American Geriatrics Society studied over two thousand people, a subset of the Hiroshima nuclear bomb survivors, whose medical histories have been tracked ever since the end of the war. It confirmed a link between previous brain injury and the development of Alzheimer's Disease. The authors did not look for any genetic links. At the same time, Nemetz et al. in the American Journal of Epidemiology examined the people with Alzheimer's Disease of the Olmstead County Traumatic Brain Injury Cohort. The section of the Olmstead County Traumatic Brain Injury Cohort that was studied were the nearly 1300 middle-aged and elderly. They discovered that when people with brain injuries develop Alzheimer's Disease, they typically do so several years before people without brain injuries do. In 2000, Baker, in Clinical Psychiatry News, reported on the work of Dr. Lindsay A. Farrer. Farrer, who used a sample of over two thousand people, stated that both previous brain injuries and the presence of the APO-e4 gene were risk factors in Alzheimer's Disease, both separately and together. However, when they were looked at separately, the presence of the APO-e4 gene was the greater risk factor than previous brain injuries. There is a hypothesis for how previous brain injuries, the presence of the APO-e4 gene, and Alzheimer's Disease are related. The anatomical features of Alzheimer's Disease are plaques (mostly made from beta-amyloid protein) and cells tangled up in balls, unlike the normal anatomy of the brain. According to the 1997 Jordan et al. study, recurrent traumatic brain injury can cause these cellular tangles, and high levels of beta-amyloid protein are often found in the brains of people who have just died from brain injuries. If someone sustains a brain injury, one or more of the precursors to developing Alzheimer's Disease are right there, waiting for a trigger to form the plaques, and to form the tangles. If that person has the APO-e4 gene, their cells' capability to repair themselves without tangling is hampered, and they already have a natural tendency to tangle. Also, APO-e4 may cause more beta-amyloid proteins than normal to remain in the brain, where they clump together to form the plaques. Although Alzheimer's Disease has gotten a great deal of press, there are other neurological disorders that affect senior citizens. The process of aging itself slowly kills off nerve cells, even if no other disorders are present. The Johnstone et al. study in 1998 in Brain Injury, looked at neuropsychological test results of over two hundred subjects of various ages, and compared them to the test results of people without brain injuries. The authors found that the combination of aging plus a previous brain injury led to greater neuropsychological impairment in senior citizens with brain injuries than in younger people who had brain injuries, when severity of injury and time since the injury were matched. They found that there was always an achievement gap in a specific age range between people with brain injuries and people without brain injuries. They also found that the decline in achievement as one looked at older and older sets of people was the same, which means that the scores, when plotted, look like parallel lines trending down and to the right. This challenged the findings in the 1996 article by Klein et al. in the Journal of Nervous and Mental Disease. Some of their tests on middle-aged people and senior citizens, both with mild to moderate brain injuries and without brain injuries, indicated that the coping mechanisms that people put into place to deal with their impaired cognitive abilities after their brain injuries fall apart as they get older. The cognitive abilities of senior citizens with brain injuries declined more rapidly than those of the senior citizens without brain injuries. Also, in some of their tests, middle-aged people with brain injuries had similar cognitive abilities to senior citizens without brain injuries. There are forms of dementia other than Alzheimer's Disease. Salib and Hillier's article mentioned above demonstrated a link between previous brain injuries and their development. The 1999 article in Pharmacopsychiatry by De Deyn et al. on vascular dementia, a disorder related to strokes, links pre-existing cognitive impairments as a risk factor in developing vascular dementia. It appears that senior citizens with brain injury may suffer from a form of brain atrophy. Filipovic and Teofilovski-Parapid's 1998 article in the Italian Journal of Anatomy and Embryology found that enlarged cava septum pellucidi, a feature associated with the development of epilepsy, mental illness, and cognitive disorders, were frequently found in the brains of senior citizens with a history of either brain injury or alcoholism. It appears that a brain injury makes the aging process even harder, with an increased risk of developing Alzheimer's Disease, non-Alzheimer's Disease-related dementia, and brain atrophy. It seems that the coping mechanisms that were set up when a person with a brain injury was younger decay as the portions of the brain that were called up to replace the injured portions age and die away. This means that senior citizens with brain injuries could have a greater need for in-home supports and other forms of specialized care. More research needs to be done to settle the questions raised here: the relationships between the various neurodegenerative disorders need to be clarified, and their relationships to previous brain injuries also need to be clarified. Neurogeriatric rehabilitation techniques need to be perfected, as life expectancies stretch closer to the century mark. References: De Deyn, PP, Goeman, J, Engelborghs, S, Hauben, U, D'Hooge, R, Baro, F, and Pickut, BA. "From Neuronal and Vascular Impairment to Dementia." Pharmacopsychiatry, vol. XXXII (Supplement): 17-24. New York: Georg Thieme Verlag, 1999. Baker, Barbara. "Head Injury Confers Alzheimer's Risk Regardless of apo E-4 Status." Clinical Psychiatry News, vol. XXVIII, no. 1: 2. San Francisco: International Medical News Group, 2000. Filipovic, Branislav, and Teofilovski-Parapid, Gordana. "Ageing changes of morphological characterisitce of cavum septum pellucidi in adults: a dissectional study." Italian Journal of Anatomy and Embryology, vol. CIII, no. 2: 107-116. Florence: Edetrice Il Sedicesimo, 1998. Graham, DI, Horsburgh, K, Nicoll, JAR, and Teasdale, GM. "Apolipoprotein E and the Response of the Brain to Injury." Acta Neurochirurgia, vol. LXXIII (supplement): 89-92. Vienna: Springer-Verlag, 1999. Johnstone, Brick, Childers, Martin K., and Hoerner, John. "The effects of normal ageing on neuropsychological functioning following traumatic brain injury." Brain Injury, vol. XII, no. 7: 569-576. New York: Taylor and Francis, 1998. Jordan, Barry D., Relkin, Norman R., Ravdin, Lisa D, Jacobs, Alan R, Bennett, Alexandre, Gandy, Sam. "Apolipoprotein E e4 Associated With Chronic Traumatic Brain Injury in Boxing." Journal of the American Medical Association, vol. CCLXXVIII, no. 2: 136-140. Chicago: American Medical Association, 1997. Kerr, Mary E., and Kraus, Marilyn. "Genetics and the Central Nervous System: Apolipoprotein E and Brain Injury." AACN Clinical Issues, vol. IX, no. 4: 524-530. Philadelphia: JB Lippincott Co., 1998. Klein, Martin, Houx, Peter J, and Jolles, Jellemer. "Long-Term Persisting Cognitive Sequelae of Traumatic Brain Injury and the Effect of Age." Journal of Nervous and Mental Disease, vol. CLXXXIV, no. 8: 459-467. Baltimore: Williams and Wilkins: 1996. Mayeux, R, Ottman, R, Maestre, G, Ngai, C, Tang, M-X, Ginsberg, H, Chun, M, Tycko, B, and Shelanski, M. "Synergistic effects of traumatic head injury and apolipoprotein e-4 in patients with Alzheimer's disease." Neurology: vol. XLV: 555-557. Hagerstown: Lippincott-Raven, 1995. Mehta, KM, Ott, A, Kalmijn, S, Slooter, AJC, Van Duijn, CM, Hofman, A, Breteler, MMB. "Head trauma and the risk of dementia and Alzheimer's disease: The Rotterdam Study." Neurology: vol. LIII: 1959-1962. Hagerstown: Lippincott-Raven, 1999. Nemetz, Peter N, Leibson, Cynthia, Naessens, James N, Beard, Mary, Kokmen, Emre, Annegers, John F, and Kurland, Leonard T. "Traumatic Brain Injury and Time to Onset of Alzheimer's Disease: A Population-based Study." American Journal of Epidemiology: vol. CIL, no. 1: 32-40. Baltimore: Johns Hopkins University School of Hygeine and Public Health, 1999. Rasmusson, DX, Brandt, J, Martin, DB, and Folstein, MF. "Head injury as a risk factor in Alzheimer's disease." Brain Injury: vol. IX, no. 3: 213-219. New York: Taylor and Francis, 1995. Salib, Emad, and Hillier, Valerie. "Head Injury and the Risk of Alzheimer's Disease: A Case Control Study." International Journal of Geriatric Psychiatry: vol XII: 363-368. Chichester: John Wiley and Sons, Ltd., 1997. Yamada, Michiko, Sasaki, Hideo, Mimori, Yasuyo, Fumiyoshi, Kasagi, Sudoh, Shinji, Ikeda, Junko, Hosoda, Yutaka, Nakamura, Shigenobu, and Kodama, Kazunori. "Prevalence and Risks of Dementia in the Japanese Population: RERF's Adult Health Study Hiroshima Subjects." Journal of the American Geriatrics Society: vol. XLVII: 189-195. Baltimore: Williams and Wilkins, 1999.
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