NEW OPPORTUNITIES FOR A BETTER QUALITY OF LIFE IN ELDERLY
Aging is one of the most significant social phenomena of the twenty-first century. The world's elderly population is growing at a rate of 2.4% per year, faster than the rest of the population and presents major challenges for society and for health services. As average life expectancies in most populations increase, so do the problems associated with age, specifically dementia and depression. Greater understanding of significant associations of successful aging is likely to help identify potentially modifiable characteristics in the individual's behavior and environment. Recently, researchers have sought direct evidence that interventions through lifestyle changes or by active treatment can improve the quality of life in elderly.
There is no satisfactory definition of the normal ageing process. It can be defined as a cumulative process of adverse changes in physiological, psychological and social functions that characterize average older people. Normal ageing as a social concept refers to an accepted range of variation in health, appearance, and performance of adults at different stages of their lives. However, it is always difficult to make a distinction between normal and pathological ageing.
Many believe that aging is the top public health problem we face today (1). This negative view of old age contrasts with some exciting empirical research on older adults who continue to function well and are aging “successfully”.
The most widely used definition of successful aging is based on objective measures used by researchers to asses freedom from chronic disease and disability, along with high physical and cognitive functioning and social engagement (1). Health care utilization and costs for older adults might be determined by such objective measures of successful aging.
The secret of successful aging is unknown; however, the aging process may begin while in utero. The distinction between “normal” senescent phenomena and age-related disease remains unclear. Human neuronal aging includes a complex mixture of atrophy, hypertrophy, synaptic reorganization, and cell death. Genetic, environmental, systemic and immunological factors may influence human brain aging. Smoking, exercise, and body mass in middle to late life predict both survival and disability. Elderly individuals with good health habits may survive longer and have a good quality of life.
MILD COGNITIVE IMPAIRMENT (MCI)
MCI is an etiological heterogeneous condition characterized by cognitive decline greater than expected for an individual’s age and education level, but that does not interfere notably with activities of daily life, subjects performing poorly on a variety of cognitive, functional and behavioral parameters, compared with normal person of the same age, but the cognitive decline is not enough severe to characterize dementia (2).
For diagnosis of mild cognitive impairment are used the Peterson criteria (2001) (2):
– memory complaint, preferably corroborated by informant,
– impairment is 1.5 standard deviations (SD) below peer norms,
– impaired memory function for age and education,
– preserved general cognitive function,
– intact activities of daily living,
– not demented.
Use of term MCI by clinicians is increasing, as they see more and more such patients in clinical settings as the populations ages and awareness of the treatability of some forms of dementia grows. According to an evidence-based medicine review, the American Academy of Neurology recommends that MCI is a useful clinical concept worthy of attention. This is because persons with MCI progress to dementia at a rate of 10% to 15% per year, which is in contrast to the normal elderly cohort that convert at 1% to 2% per year (3). The transition is usually to Alzheimer’s dementia, and less commonly to vascular dementia. In referral clinic populations, most patients with a diagnosis of mild cognitive impairment either persist with mild cognitive impairment or progress to dementia, and on autopsy such patients have characteristic neuropathological findings of Alzheimer’s disease, including senile plaques (4). Today, MCI is considered to be a prodromal stage of dementia (5).
ETIOLOGY OF MCI
The cognitive decline etiology includes genetic factors and environmental factors (viral infections, food, smoking, stress).
Fat diet increases the risk of disease. Depression is secondary to stress, and untreated depression is a major risk factor for cognitive impairment and for dementia (3). Another risk factors for mild cognitive impairment are: cardiovascular disease, abnormal blood pressure, too high or too low, metabolic disorders, low levels of physical, social and mental activity, fewer years of education. People who have higher levels of social, mental and physical activity seem to have less risk of MCI and dementia.
Dementia is more prevalent in women than in men. A large amount of this difference is explained by the greater life expectancy of women and by a higher survival rate of women with dementia when compared with same- age men with dementia (5, 6).
Early-onset dementia is more common in individuals with a family history of dementia. In addition to its association with atherosclerosis, the apolipoprotein E (APOE) gene is acknowledged to be associated with dementia and, in particular, with a risk for Alzheimer disease. APOE allele distribution varies across the world. The ε4 allele is most common in areas of the world where the food supply is currently or has recently been scarce, and is lowest in southern Europe, the Middle East, and North Africa (6). This finding is consistent with research showing that APOE genotype determines the effects of dietary and other risk factors on the risk of dementia (6, 7).
Cerebrovascular disease is commonly observed in post-mortem studies of persons with dementia and, therefore, the risk factors that have been established for vascular disease are assumed to affect the risk of dementia. Vascular risk factors are also commonly associated with an increase in the risk of Alzheimer disease (5, 6).
There is evidence that after adjustments for comorbid conditions, midlife obesity (defined a body mass index greater than 30 during ages 40-45 years) was a risk factor for dementia in old age and being overweight (body mass index of 25-30) also increased risk (5). Adherence to a Mediteranean diet has been consistently associated with improved cardiovascular health and with a reduction in the risk of dementia (8).
Prospective studies have found that moderate intake of alcohol (specifically wine) is associated with halving on dementia risk. However, the interactions between drinking, diet and social activity are often not take into account and may explain this association (7, 8). Several prospective studies have reported an increase in dementia risk with low high-density lipoprotein (HDL) cholesterol and high low-density lipoprotein (LDL) cholesterol. High total cholesterol in midlife is also associated with increased dementia risk (7). Prospective studies consistently report no difference in risk between individuals who use statin drugs and those who do not (6).
A systematic review found consistent evidence that diabetes both in midlife and later life is a risk factor for both Alzheimer disease and dementia in general (5, 6, 7). Effective control of diabetes may reduce the risk.
The early controversy surrounding the effect of smoking on the onset of dementia has now been set aside, with prospective studies consistently finding either no effect or evidence of increased risk of dementia or cognitive decline in smokers (6, 7).
Both current depression and a history of depression are associated with a doubling of the risk of dementia (5, 6, 7).
Discovering risk factors helps to identify who is most at risk of a disease, enables the development of strategies for primary and secondary prevention, and helps to understand the underlying pathologies. Risk factors for incidence are also risk factors for prevalence, so understanding the effects of risk factors will help to predict how the disease burden in a population will respond to demographic or cultural changes and to design interventions for primary prevention.
Recently, researchers have sought direct evidence that interventions through lifestyle changes or by active treatment can reduce the risk of dementia.
PREVENTION OF MCI
The primary prevention of MCI involves the prevention of the appearance of the disease by measures applied to the individual and the environment (7). The treatment of risk factors includes the treatment of h y p e r t e n s i o n , h y p e r c h o l e s t e r o l e m y, d i a b e t e s , hypothyroidism, depression, sleep disorders and other psychiatric disorders that may adversely affect cognitive status.
In addition to the specific treatment related diseases mentioned above, MCI’s primary prevention includes physical activities, alcohol in moderation and Mediterranean diet. Other non-pharmacological interventions which may have effects on memory and their removal are: stress factors, sleep low, taken medication (anticholinergic and sedative).
Regular physical activities seems to improve the memory loss to persons over 50 years with cognitive impairment, according to a study done in Australia, publicized in Journal of the American Medical Association in 2008 (7).
Recent research has shown that diet plays a major role in preventing cognitive impairment and reducing the risk of MCI conversion to AD. Mediterranean diet is currently considered the most healthful diet because high intake of fruits and vegetables. Mediterranean diet contains large amounts of beta-carotene, vitamin C, tocopherols, tocotienoli (vitamin E), polyphenols and essential minerals such as selenium, magnesium, zinc, iron, calcium and iodine) (8).
CONTROL OF CARDIOVASCULAR RISK FACTORS
Arterial hypertension is a risk factor for mild cognitive impairment. Multiple mechanisms has been proposed to explain the correlation between arterial hypertension and MCI. Arterial hypertension is a risk factor for cerebrovascular diseases, and these are risk factor for MCI.
The goal is to slow cognitive stimulation rate of cognitive decline using functional approaches in order to strengthen cognitive function (2). In art therapy it is possible to express ideas and feelings that cannot be converted in wordsan this is important for people with language impairment.
Art therapy have been used initially in Germany in the rehabilitation program of patients diagnosed with early dementia (9). Art therapy is a nonverbal form of therapy that uses visual imagination. In art therapy it is possible to express ideas and feelings that cannot be converted in words. This is important for people with language impairment.
Secondary prevention lies in identifying and treating asymptomatic or presymptomatic persons having a risk factor of developing the disease; if MCI, secondary prevention can be achieved by use of anti-aging treatment, such as: omega-3 acids, natural products on herbal (vinpocetinum, Rhodiola Rosea, gingko-biloba), nootropics (piracetam), antioxidants (vitamin E, vitamin C, vitamin A, alpha-lipoic acid, Coenzyme Q10).
An alternative method consists in the administration of extracts of Rhodiola Rosea strain containing bioactive alkaloids, polyphenols and phenylpropanoids. The effects on the brain function are: cognitive stimulation, memory improvement, learning improvement and improvement of abstraction capacity (10). The effects of Rhodiola Rosea are augmented in combination with Piracetam or Ginseng.
Antioxidants (vitamin E, Vitamin C, Vitamin A, alpha-lipoic acid, Co-enzyme Q10) are substances which may protect brain cells from the oxidative stress (11). The oxidative stress plays a role in Alzheimer’s, but there’s little evidence that either is effective in preventing MCI from progressing to dementia.
Ginkgo biloba has been used medicinally for thousands of years. Ginkgo has been used even as treatment and as dietary supplement in Europe and in Asia. Ginkgo is used for the treatment of numerous conditions, many of which are under scientific investigation (12). Ginkgo biloba has antioxidant properties and inhibit the formation of β-amyloid protein with a role in forming amyloid plaques in patients with dementia. Administered in a dose of 40 mg three times a day ginkgo improve the cerebral flow (12).
At least one randomized, placebo-controlled, duble-blind, multi-center trial indicates that vitamine E may delay the progression of moderate-to-severe AD (13), but, the research is still underway to determine its efficacy in MCI. The combination supplemental of vitamin E (400UI/day or more) and vitamin C (at least 500mg/day of ascorbic acid) but not either vitamin alone reduce significantly the incidence and prevalence of dementia. The administration of vitamin E in combination with selegiline delays the institutionalization and the progression of dementia. There are clinical trials looking at vitamin E plus selegiline (a mono-amine-oxidase inhibitor) as a treatment for dementia and for preventing progression of cognitive impairment (3).
Nootropics are drugs that boost brain activity and memory and enhance the brain function. Piracetam is the most used nootropic, increases performance in a variety of cognitive tasks, appear to be effective in dementia and mild cognitive impairment. The dose of piracetam used for cognitive decline is 1600mg/day and the side effects are few, transient and mild.
Anti-inflammatory agents have role in reducing inflammation in the brain as having a role in reducing risk for cognitive deterioration. Researchers and clinicians have shown that individuals who consumed NSAIDs have a reduced risk of dementia, taking non-steroidal inflammatory (ibuprofen) taken over two years decreased risk of Alzheimer’s dementia. Other studies have demonstrated the effectiveness of aspirin and acetaminophen, rofecoxib (cyclo-oxygenase 2 inhibitor) had comparable effects with ibuprofen administration (11).
HORMONAL TREATMENT IN MCI
Replacing the estrogen lost at menopause can prevent many of the manifestations of aging including osteoporosis, cardiovascular disease and decline in cognitive functions. Hormone replacing therapy after menopause have benefits for menopausal symptoms, for cognitive function – neuroprotective inhibit neuronal apoptosis and modulate Apolipoprotein gene expression (3).
Cholinesterase inhibitors are typically used to treat the early and middle stages of dementia. Alzheimer disease treatment can be extrapolated and used for mild cognitive impairment. This is because the deterioration in the production of acetylcholine accelerates over time, as more and more brain cells become damage did. These include donepezil, rivastigmine, galantamine and tacrine. Cholinesterase inhibitors are used for long term treatment. Cholinesterase inhibitors improve or at least retarding the rate of loss of cognition, the drugs can improve a person’s quality of life.
Tertiary prophylaxis prevents association factors that lead to disease, preventing complications from occurring
There is a multifactorial model of successful aging with interacting components including physical functioning and risk, activity, social engagement and psychological traits.
Greater understanding of significant associations of successful aging is likely to help identify potentially modifiable characteristics in the individual’s behavior and environment.
Taking into account the fact that the mild cognitive impairment is considered as a prodromal phase of dementia, it is important to identify it early and to start the primary prevention. The primary prevention refers to the specific treatment of cognitive features and to changes of the lifestyle. Early detection and the treatment of mild cognitive impairment can maintain the elderly at a maximum level of functionality as much as possible.
1. Dilip V, Jeste MD, Gauri N et al., Association between older age and more successful aging: crtical role of resilience and depression. Am J Psychiat 2013;170 (2): 133-240.
2. Petersen RC. Aging, mild cognitive impairment, and Alzheimer’s disease. Neurol Clin 2000.
3. Agronim EM. Alzheimer Disease and other dementias, Second
Edition. Lippincott Wiliams and Wilkins, 2004.
4. Belleville S, Lepage E, Bhere L, Chertrkow H and Gauthier S. Measures of executive functions and working memory in older persons with mild cognitive impairment. Paper presented at the ninth Cognitive Aging Conference , Atlanta, GA, USA, 2002.
5. Dubois B, Feldman HH, Jacova C et al. Revising the definition of
Alzheimer disease: a new lexicon. Lancet Neurol 2010; 9(11): 1118-
6. Myron F, Weiner MD, Lipton AM. Textbook of Alzheimer Disease and
Other Dementias. American Psychiatry Publishing, 2012.
7. Lautenschlager NT, Cox KL, Flicker Let al. Effect of physical activity on cognitive function in older adults at risk for Alzheimer disease: a arandomised trial. JAMA 2008;300(9): 1027-1037.
8. Scarmeas N, Stern Y, Mayeux R et al. Mediterranean Diet and Mild
Cognitive Impairment. Arch Neurol 2009;66(2): 216-225.
9. Moniz-Cook E, Manthorpe J. Early Psycosocial Intervention in Dementia, Evidence Based Practice. London and Philadelphia: Jessica Kingsley publishers, 2009.
10. Tasman A, Kay J, Lieberman JA et al. Psychiatry. Third Edition. London: John R. Wiley and Sons, 2008.
11. Spar JE, La Rue A. Clinical Manual of Geriatric Psychiatry. Washington DC: American Psychiatric Publishing, Inc, 2006.
12. Birks J, Grimley Evans J. Ginkgo biloba for cognitive impairment and dementia. Cochrane Database Syst Rev 2007;18(2):CD003120.
13. Sano M, Ernesto C, Thomas RG et al. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer’s disease. The Alzheimer’s Disease Cooperative Study. N Engl J Med 1997;336(17):