What happens to our brain as we age? Are a fading memory and difficulty learning “new tricks” inevitable outcomes as we enter into our golden years? More seriously, are we all bound to develop Alzheimer’s disease or some other form of dementia if we live long enough? As Americans in general are enjoying a longer lifespan, the maintenance of a healthy, working brain becomes even more important. Partly driven by advanced technology, a significant amount of research is being conducted to gain a better understanding of the diseases of dementia among the elderly. Some efforts have proven frustrating, such as in the domain of medical treatments for dementia. However, significant advances have been made in better understanding the causes and possible prevention of cognitive disorders. Until recently, existing models of cognitive aging suggested an unavoidable decline, a decline mostly attributed to structural damage (e.g., brain cell loss). On the contrary, current research is pointing to a significant level of variation among the brain capacity of elderly individuals. Studies are being conducted on those individuals who show no slowing down of their cognitive faculties in an attempt to determine what resilient factors these individuals possess that keeps them mentally sharp throughout their lifetime.
What is Cognitive Aging?
Cognitive aging refers to a pattern of age-related changes of cognitive functioning. Although this declining trend has been thought to begin as early as the mid-20’s, most agree that mild cognitive changes can be noticed in the 40’s and progress throughout the 50’s and beyond. Common problems include forgetfulness, word finding difficulty (also termed “tip-of-the-tongue phenomenon”), slowed reaction time and difficulty learning new tasks.
The importance of maintaining optimal cognitive health appears to be even more important than previously recognized. In a recent longitudinal study on almost 2000 non-demented individuals aged 65 and older, rate of decline in cognitive and functional skills is one of the strongest predictors of mortality (Schupf et al., 2005). One reason they offer for this phenomenon is that decreased cognitive ability leads to reduced activation and less engagement in activities of daily living. The increased rate at which cognitive problems emerge among the aging emphasizes the importance of better understanding the cognitive problems, as detailed in the chart below:
Does Everyone Develop Cognitive Problems as they Age?
A large percentage of the elderly will go on to develop cognitive problems. Some studies indicate that, after age 80, up to 50% of individuals will have Alzheimer’s disease. That statistic is particularly sobering given the fact that many more are living well into their 80’s. Although specific cognitive diseases are a distinct phenomena, we cannot assume that cognitive decline is an inevitable outcome. In fact, there is a significant amount of variability among the cognitive capacity of older individuals. Whereas it was previously thought that cognitive decline is a slow, insidious process that most of us will face, Wilson et al. (2002), for example, found that there was little age-related cognitive decline among the individuals he sampled unless they were tested within a few years of their death. Indeed, health problems are a profound concern among the elderly and strike at an inordinate rate compared with their younger counterparts, as detailed in the graph below:
Furthermore, there are many elderly individuals who never develop cognitive problems, even among the oldest-old. In a retrospective study of New England centenarians aged 100 to 198, 89% were still living independently at age 93, 73% at age 97, and 35% at 102 (Hitt et al., 1999). In other words, these individuals were not demented and continued to engage in an active lifestyle.
What are the different types of cognitive disorders among the elderly?
In response to the growing concern with cognitive aging and the public demand for better diagnosis and treatment, aging specialists have worked towards developing a conceptual model of cognitive aging across a continuum. This effort is particularly important in that it can help people identify potential problems at an earlier stage when more effective interventions can occur. Also, it will help the ongoing research to better understand just how dementia occurs. The hope is that early intervention and better understanding of patterns of decline will ultimately prevent or reduce the impact of dementia.
I. Age-associated Memory Impairment (AAMI)
Many authorities consider cognitive decline to be a normal consequence of aging. Over the age of 50, mild memory changes may occur while other cognitive functions remain intact. The problem is usually experienced as mildly to moderately troublesome to the individual but not always observable to others. On average, individuals with AAMI will score one standard deviation (SD) below average on memory tests, when compared against younger norms. Performance on other tests of cognitive function is relatively intact. AAMI prevalence rates are estimated at 18.5% of those 50 and over, increasing to 38% between ages 60-78.
II. Age-Associated Cognitive Decline (AACD)
Age-Associated Cognitive Decline is a term used to capture those individuals whose cognitive problems include the memory difficulties of AAMI but also extend to such cognitive domains as language, visuospatial ability and executive function. As in AAMI, test performance is approximately one SD below younger norms. In order to meet diagnostic criteria for this category, the problem must have been present for at least six months (Levy, 1994). AACD rates have been reported to be 9% after age 75 (Busse et al., 2003) and up to 35% at age 60 and over (Richards et al., 1999). It is not clear that AACD will lead to dementia, but symptom presentation marks an extremely important time to seek medical and psychological attention. People sometimes believe they are having memory problems when there are no actual decreases in memory performance. Therefore, assessment of cognitive function requires specialized professional evaluation.
III. Mild Cognitive Impairment (MCI)
Mild Cognitive Impairment describes the slight impairment in cognitive function—typically memory—that is thought to be a transitional state between the cognition of normal aging and mild dementia (see criteria box). Individuals will test 1.5 SD below peer norms (people their own age, as compared with AAMI and ARCD, in which they are below younger norms).
Prevalence rates of MCI vary somewhat because different studies use slightly different criteria. Roughly, the prevalence of MCI ranges from 3-6%. Researchers suggest that 10-15% of individuals with MCI will progress onto AD per year, compared to 1-2% per year when sampled from the general population.
The term “dementia” is often confusing because most people think of dementia as only Alzheimer’s disease. In fact, dementia is a general term that describes a syndrome of acquired persistent dysfunction (2 or more SD below peers) in two or more cognitive domains that can include memory, language, visuospatial ability and executive functions (e.g., planning, cognitive flexibility, executing specific tasks). The onset can be abrupt, as in stroke, or gradual, as in Alzheimer’s disease. Dementia affects nearly 5% of the population over age 65.
Alzheimer’s disease (AD) is the most common of the dementias, affecting approximately 3% of the population between the ages of 65 and 74 and increasing to nearly 19% between 75 and 84. The incidence may increase to 50% after 85. Primary cognitive problems of AD include memory impairment, language disturbance (aphasia), visuospatial deficits and impaired executive function. The ability to form new memories is particularly compromised as well as one’s ability to organize, plan and strategize (executive function). EEG testing may show excessive theta wave activity, and MRI studies will show overall brain shrinkage (atrophy). There is reduced blood flow to the cortex.
Dementia with Lewy Bodies is often under-recognized. It affects both the cortex and subcortical structures. The most prominent symptoms include psychosis (e.g., delusions, visual hallucinations), disinhibition and symptoms of Parkinsonism (e.g., rigidity, difficulty moving). Deficits include problems with attention/alertness, executive functions and visuospatial functions.
Frontotemporal dementia (e.g., Pick’s disease), another dementia that affects the cortical layer first, is characterized by significant changes in personality and behavior (e.g., apathy, disinhibition/social misconduct, mood changes, lack of empathy, poor judgment) in addition to cognitive decline.
Subcortical dementias involve underlying brain structures such as the basal ganglia, thalamus and cerebellum. In addition to cognitive disturbances of attention, visuospatial ability, memory and executive function, these dementias are often distinguished by movement disorders, in which individuals have difficulty walking or demonstrate an observable tremor. The major disorders in this category include Parkinson’s disease and Huntington’s disease.
Vascular Dementia (VaD) results from ischemic cerebral injury such as would occur in a heart attack, stroke or other disease process that affects circulation (e.g., high blood pressure, congestive heart failure, diabetes). VaD is the second most common dementia, accounting for 12-20% of all the dementias. Characteristics of this disorder are dependent upon the location of cerebral damage. In contrast to AD, onset of symptoms tends to be abrupt and often related to a specific incident such as a heart attack or stroke. Instead of gradual decline, the cognitive impairment change is stepwise in fashion. Also, there may be a fluctuation in symptoms.
What causes cognitive decline?
The exact cause of cognitive aging is not fully understood. Although in the past there was an assumption that aging resulted in an inevitable breakdown of neurons, and therefore, cognitive capacity, the data show that there is a restrictive loss of neurons in only a few areas. It seems that breakdown in the critical junctions for synaptic communication seems to be the most likely culprit in cognitive decline. Synaptic communication can be disrupted when the delicate neurochemical balance of the brain is compromised. For example, it is well known that excessive amounts of stress produce a hormone known as cortisol. High amounts of cortisol can be deadly to the specialized cells positioned in the hippocampus, a part of the brain devoted to learning and memory formation. Oxidative stress is another important contributor to age-related neuronal breakdown and is often observed in increasing concentrations in individuals with dementia and Alzheimer’s disease.
Although many of us are not as wise at that age (wisdom being a cognitive function that actually improves over the years), younger brains tend to process information at a quicker rate and can learn new activities much more quickly. Speed, or more specifically, processing speed, has been identified as a primary factor in poorer cognitive performance among the aged. In cognitive slowing, there is a decrease in the rate at which mental operations occur, and this would have an overarching impact on everything else. For example, if an older person is listening to instructions, their slower ability to process the information impedes their learning. Therefore, it is not so much that they cannot learn, but that they would need more time. Others have argued that older people have more difficulty planning, organizing and solving problems, lacking the optimal “executive functioning” that allows for fluid reasoning and creative, innovative problem-solving (May, Hasher, & Kane, 1999). The physical region that manages these tasks is the frontal cortex positioned in the very front of the brain. Still others have argued that decreased sensory function of an aging brain with reduced vision, smell and hearing, is a sign of poor overall neurological health with negative impacts on cognitive performance (Baltes & Lindenberger, 1997; Lindenberger & Baltes, 1994).
Although the above discussion explores the features of the aging brain, it does not explain “how” the brain ages. Is it a structural breakdown of neurons that displays itself in plaques and tangles, such as in AD, or is it more related to change in function?
Disconnection Syndrome- A New Look at Cognitive Impairment in the Elderly — or a new look at “if you don’t use it, you lose it.”
Researchers are taking a second look at the aging brain. The discovery of tangles (neurofibrillary tangles) and plaques (amyloid) in the brains of deceased Alzheimer’s patients reinforced the notion that structural damage was solely responsible for the cognitive problems observed when they were alive. Surely, a great quantity of neuronal damage in key brain areas, like the hippocampus, would negatively impact brain function. But it is not that simple. Tangles and plaques have been found upon autopsy in the brains of individuals who showed no deterioration of cognitive function. The central nervous system can continue to function adequately despite structural breakdown. Some researchers are now examining the brain more from its function and communication ability rather than its structure. In this approach, it is the functional interaction between different brain systems that matters more, and certain brain regions, such as the prefrontal cortex and hippocampus, are particularly important players. Therefore, it is the communication/integration of different brain pathways that seems to matter more and can better point to the quality of brain function, despite age. O’Sullivan et al. (2001) studied the communication fibers (white matter) in the brains of younger and older subjects. The researchers found that there was a significant difference between the two groups, with the younger groups showing more robust connectivity between different brain areas. However, it should be noted that—though overall the younger subjects showed higher density of white matter fibers—there was significant variation in the older subjects, up to the age of 80. This suggests that while we all start out pretty much on a level playing field, individual differences become more apparent as we age. According to the communication theory, the tangles and plaques at key communication junctions are more of a byproduct of reduced communication than as the cause itself, and the brain is looked upon more as a dynamic agent than an organ composed of disparate parts. Given this, how can we improve communication in the brain and how can we stimulate it to become more active and engaged in its environment?
Coherence is a term used to describe the functional connection between two or more cerebral areas and has been used to measure the extent to which different brain regions are communicating. Quantitative Electroencephalography (QEEG) is a technology that can measure coherence levels in the brain. Leuchter et al. (1992) found that individuals with AD and multi-infarct dementia (MID) had lower coherence levels in specific brain pathways.
What this means is that instead of structural breakdowns, there is instead a progressive worsening of connectivity between cerebral areas that sub-serve these functions. In fact, the connectivity function in the brain is part of a theory that is gaining greater acceptance in scientific circles and may perhaps even usher in a whole new host of pharmacological agents. In this view, the timing of brain activity, rather than its structural and neurochemical status, seems to be more related to states of health and disease.
What this means is that instead of focusing on just structural breakdowns in specific clusters of neurons and areas of the brain, we should focus more on the progressive worsening of connectivity between cerebral areas that sub-serve these functions. In fact, the connectivity function in the brain is part of a theory that is gaining greater acceptance in scientific circles and may perhaps even usher in a whole new host of pharmacological agents. In this view, the timing of brain activity and communication among neurons may be more related to states of health and disease than the mere structural integrity of neurons. Combining these two views would suggest that we should not only continue to research the abnormality of specific structures within neurons (e.g., neurofibrillary tangles) and close to neurons (e.g., plaques) but should also research the connectivity among neurons, including the timing of neuronal firing and the neurochemistry that sub-serves that firing.
In sum, there is a growing body of scientific research suggesting that cognitive disorders in the elderly are strongly influenced by the functional, communicative aspects of the central nervous system and less so related to a disease-based, structural-damage model. Effective treatments for MCI and the dementia spectrum continue to pose one of the greatest challenges in the medical field. Although pharmaceutical treatment is available, the drugs seem to only stave off cognitive decline for a brief time. Despite the significant amount of effort being directed towards research into the causes and treatment for cognitive disorders, we are nonetheless still faced with a growing problem in the aging population.
In sum, there is a growing body of scientific research suggesting that cognitive disorders in the elderly are strongly influenced by the functional, communicative aspects of the central nervous system and less so related to a structural-damage model. Effective treatments for MCI and the dementia spectrum continue to pose one of the greatest challenges in the medical field. Although pharmaceutical treatment is available, the drugs seem to only stave off cognitive decline for a brief time. Despite the significant amount of effort being directed towards research into the causes and treatment for cognitive disorders, we are nonetheless still faced with a growing problem in the aging population.
Is Cognitive Decline Inevitable?
The Seattle Longitudinal Study of Adult Intelligence has followed a group of more than 5000 people for well over four decades. The program began in 1956, and participants have been tested across a whole gamut of mental and physical abilities at seven-year intervals since that date. The study produced a number of important findings as follows:
Research into aging and cognition strongly suggests that maintaining an active cognitive lifestyle is important. It can delay onset of cognitive decline or perhaps even prevent it altogether. There are a number of positive steps you can do to make changes RIGHT NOW that can help you in the years to come. Outside of healthy steps you can take on your own (see article on Steps for Healthy Aging), professional help is also available. The Brain Therapy Center offers a full spectrum of psychological services for the detection and treatment of cognitive problems. If you are not sure of your current cognitive status, you can undergo comprehensive neuropsychological evaluation. If cognitive problems are detected, Dr. Burke and Dr. Andreoli will design a specialized neuropsychological rehabilitation (NR) program designed to remediate your problem. The training will likely include cognitive rehabilitation (CR) and Neurofeedback (NF), which can work synergistically to target your problems. (See Neuropsychological Rehabilitation and Neurofeedback under Services.) Neuropsychological rehabilitation offered at the Brain Therapy Center is designed to specifically target the very problems that have been found to develop in the aging brain and are particularly suited to the concepts discussed in the “disconnection syndrome.” If you require additional treatment in the form of a physical therapy regimen or nutritional program, we can refer you to qualified providers within our integrative network.
At present, there is no cure for AD and other forms of dementia, once they have developed to the point where they can be identified. However, the inevitability of ARCD and MCI are not so easily defined and in fact may be reversible. It is of utmost importance to obtain treatment at the earliest stage in order to make the necessary changes that can offset a decline along the dementia continuum. Taken together, the combination of NF and CR offers a synergistic approach that both stimulates the brain and provides directed feedback to consolidate the activation of specific brain circuitry that is devoted to learning. NF and CR, both offered at the Brain Therapy Center, can serve to enhance cognitive function. Contact the Brain Therapy at (805) 449-8777 to speak with Dr. Andreoli or Dr. Burke if you have any questions or would like to schedule an appointment.
Bennett, et al. (2005). Perceived social support as a predictor of mortality in coronary patients. Effects of smoking, sedentary behavior, and depressive symptoms. Psychosomatic Medicine, 67, 40-45.
Bosworth, H. B., & Schaie, K. W. (1997). The relationship of social environment, social networks, and health outcomes in the Seattle Longitudinal Study: Two analytical approaches.Journal of Gerontology: Psychological Sciences, 52B, 197-205.
Busse, A., Bischkopf, J., Riedel-Heller, S.D. (2003). Mild cognitive impairment: prevalance and incidence according to different diagnostic criteria: Results of The Leipzig Longitudinal Study of the Aged (LEILA75+). British Journal of Psychiatry, 182, 449-454.
Dreary, I.J., (2000). Looking down on human intelligence. Oxford University Press, Oxford, U.K.
Hitt, R., Young-Xu, Y., Silder, M., Perls, T. (1999). Centenarians: the older you get, the healthier you have been. Lancet, 354, 652.
Krugman, Herbert E. "Brain wave Measures of Media Involvement." Journal of Advertising Research 11.1 (1971): 3-9.
Levy, R. (1994). Aging-associated cognitive decline. International Psychogeriatrics, 16, 129-140.
Mulholland, Thomas, and Erik Peper, "Occipital Alpha and Accomodative Vergence, Pursuit Tracking, and Fast Eye Movements." Psychophysiology 8.5 (1971): 556-575.
O’Sullivan, M., Jones, D., Summer, P., Morris, R., Williams, S., & Markus, H (2001). Evidence for cortical “disconnection” as a mechanism of age-related cognitive decline. Neurology, 57, 632-638.
Richards, M., Touchon, J., Ledersert, B. et al. (1999). Cognitive decline and aging: Are AAMI and AACD distinct entities? International Journal of Geriatric Psychiatry, 14, 534-540.
Schupf, N., Tang, M., Albert, S., Costa, R., Andrews, H., Lee, J., and Mayeux, R. (2005). Decline in cognitive and functional skills increases mortality risk in nondemented elderly. Neurology, 65, 1218-1226.
Snowdon, D.A., Greiner, L.H., Mortimer, J.A., Riley, K.P., Greiner, P.A., Markesbery, W.R. (1997) Brain infarction and the clinical expression of Alzheimer’s disease: The Nun Study. JAMA, 277, 813-817.
Whalley, L.; Deary, I.; Appleton, C.; & Starr, J. (2004). Cognitive reserve and the neurobiology of cognitive aging. Aging Research Reviews, 3, 369-382
White, L., Petrovitch, H., Hardman, J., Nelson, J., Davis, D., Ross, G., Masaki, K., Launer, L., Markesbery, W. (2002). Cerebrovascular pathology and dementia in autopsied Honolulu-Asia Aging Study participants. Annals of the New York Academy of Science, 977, 9-23.
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