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The Aging Skin

The Aging Skin

Teaser: 

The weekend prior to my writing this editorial, skin was featured prominently in the Sunday New York Times magazine. However, the articles were more like a commentary on society than a treatise on skin care. One article concentrated on plastic surgeons and how their major interventions were now nonsurgical and focused on skin. Botox (botulinum toxin) injections, collagen injections and dermabrasion procedures were reported as being more commonly performed by plastic surgeons than their previous mainstays: breast augmentation and liposuction. One surgeon commented on how advances in science had improved the field of cosmetic surgery, such that face-lifts, in particular, were no longer required. Several seemed inordinately proud of the recent publication (as yet unverified) that stem cells could be isolated from fat cells harvested by liposuction. The second article talked about the New York dermatologist who helped popularize Botox injections. It mentioned her indulgent life style, by extension making her procedure seem indulgent as well.

However, skin is not just a cosmetic organ. As our largest organ, it is vital to our health, and serious diseases of the skin are not uncommon. The elderly are particularly prone to these diseases and accurate diagnosis and management are important. Dr. Lester discusses Bullous Pemphigoid, a serious blistering disease that is almost exclusively seen in the elderly. Recent studies have expanded the treatment options for this condition. Skin cancer is also more common in the elderly, at least partially because of longer exposure to the sun. Dr. John Adam of Ottawa discusses this topic in detail. Dr. Scott Murray tackles the ubiquitous, but challenging, problem of dry skin in the elderly. Skin manifestations of systemic illness are also very common in the elderly, and the dynamic duo of Dr. Gary Sibbald and Dr. Madhuri Reddy address the topics of pressure ulcers and diabetic foot ulcers.

Also in this issue is an article by Cynthia Westerhout and Eric Boersma, from the Department of Cardiology at the University Hospital Rotterdam and the University of Alberta on glycoprotein IIb/IIIa in percutaneous coronary intervention. This is one of those areas where basic science investigations (in this case, on platelet function) rapidly led to important therapeutic advances.

When I saw Dr. Chris MacKnight's article on acetylcholinesterase inhibitors in the treatment of Dementia with Lewy Bodies, I thought of a chart review I had just completed on a patient (not mine) who had died in hospital. When looking at the entire chart, it was obvious that the patient's confusion with fluctuating course, Parkinsonism and falls were likely secondary to this disorder, but the diagnosis was not made. There is now solid evidence that this disorder is common and can be diagnosed reasonably accurately (e.g. data from Bristol, UK). Unfortunately, there is also evidence that in most places the diagnosis is not made accurately (neither specific nor sensitive). As therapy for this disorder evolves, accurate diagnosis will be vital to ensure that our patients benefit.

Finally, Dr. Rory Fisher, Director of the Regional Geriatric Program of Metropolitan Toronto, has contributed an excellent article on the role of specialized geriatric services in acute hospitals.

In response to last year's readership survey, the next issue will focus on Nutrition in the elderly. We'll also announce the prize winners from this year's survey. Remember to look for your name!

Enjoy this issue.

The Biological and Cognitive Effects of Estrogen on the Aging Brain

The Biological and Cognitive Effects of Estrogen on the Aging Brain

Teaser: 

Elise J. Levinoff, BSc1,2, Howard Chertkow, MD, FRCPC1,2,3
1Bloomfield Centre for Studies in Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, McGill University
2Department of Neurology and Neurosurgery, McGill University
3Division of Geriatric Medicine, Dept. of Medicine, Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, PQ.

Alzheimer disease (AD) is a neurodegenerative disease of elderly patients, pathologically characterized by the presence of senile plaques and neurofibrillary tangles in the brain. This pathology occurs in the cerebral cortex, specifically within the temporal lobes, resulting in impairment in cognitive domains such as short-term memory, attention, semantics, as well as aphasia and apraxia.1 Patients also show marked changes in behaviour and are impaired in activities of daily living (ADLs). The causes of AD are unknown, but age is a major risk factor. Women are at a higher risk of developing AD, although this may be due, in part, to increased longevity. Additionally, mechanisms of neuronal injury, such as the presence of cerebral infarcts and consequences of head trauma, increase the risk of developing AD. Expression of the APOE-e4 genotype has also been associated with an increase in the risk of developing AD.1

Presently, there is no cure for AD.

Aging and the Neurobiology of Pain

Aging and the Neurobiology of Pain

Teaser: 

Keith B.J. Franklin, PhD
Professor, Department of Psychology, McGill University, Montreal, QC.

Frances V. Abbott, PhD
Professor, Department of Psychiatry, McGill University, Montreal, QC.

 

Chronic pain afflicts a majority of persons over the age of 60 and a large proportion of those afflicted receives little or no treatment. Many of the long-term conditions that limit activity involve pain, although recognition of pain in primary care settings is complicated by the fact that stoicism tends to increase with age, and older people tend to focus on acute pain and under-report chronic complaints.1 Activity limitation, as a health indicator, has improved over the past twenty years for non-institutionalized Canadians in the 45-64 and 65-74 age groups (from 19 to 16% and 33 to 22%, respectively). In contrast, the prevalence of activity limitation in those over 75 has remained stable at around 35%. The most significant painful conditions that limit activity, arthritis and rheumatism, have remained stable over the past 20 years with an incidence of about 50% for women and just over 30% for men aged 65 and over.2

In light of the prevalence of pain in the elderly, it is surprising how little is known about the influence of age on the neurology and pharmacology of pain.

Neuroplasticity and How the Brain Adapts to Aging

Neuroplasticity and How the Brain Adapts to Aging

Teaser: 

Mark P. Mattson
Laboratory of Neurosciences,
National Institute on Aging Gerontology Research Center, and
Department of Neuroscience,
Johns Hopkins University School of Medicine,
Baltimore, MD, USA.

 

As in other industrialized countries, as the average age of the population increases, the number of Canadians that suffer from neurodegenerative conditions such as Alzheimer disease (AD), Parkinson's disease (PD) and stroke is rapidly increasing. On a more positive note, the number of people that enjoy a healthy brain as they age is also increasing. The genetic and environmental factors that determine how the brain adapts to aging are beginning to be identified, and their mechanisms of action at the cellular and molecular levels are being elucidated. Although degeneration and death of neurons occur in some brain regions during normal aging, the brain is able to adapt to the cell loss by increasing the growth and synaptic connections of the remaining neurons.1 In contrast, age-related neurodegenerative disorders occur when the death of neurons is accelerated and adaptive responses are impaired or overwhelmed. During the early years of life, the brain has a remarkable ability to adapt to adversity, such that although large regions of the brain may be damaged, normal function can be restored.2 As we age, the brain loses its ability to adapt to an insult.

Aging, Cognition and Circadian Rhythms

Aging, Cognition and Circadian Rhythms

Teaser: 

Lynn Hasher, PhD
David Goldstein, PhD
Baycrest Centre for Geriatric
Care and University of Toronto,
Toronto, ON.

Introduction
A variety of important biological, physiological and psychological functions show regular peaks and declines across 24-hour cycles. Such rhythms are present in plants and animals, from the cellular level to the level of organs and even entire organisms.1 The characteristics and implications of these circadian rhythms have been the focus of a growing body of literature in the fields of chronobiology, chronopathology and chronotherapy. For example, because of underlying circadian rhythms in cortisol concentration in the blood stream, histamine, epinephrine, pulse rate, blood pressure and clotting factors, treatment efficacy varies with the time of administration for diseases such as arthritis, asthma, cancer and cardiovascular disease.2-5 Recent work in the newly emerging area of chronocognition also shows that behavioural efficacy varies depending on the time of administration of tasks.6 Of special relevance is the clear suggestion of age differences in circadian arousal patterns, differences that raise a number of important issues for both research and clinical practice, including what patients are likely to understand and remember from a medical appointment.

The Global Aging Phenomenon and Health Care

The Global Aging Phenomenon and Health Care

Teaser: 

Alexandre Kalache, MD, PhD,
Chief, Ageing and Life Course (ALC),
World Health Organization,
Geneva, Switzerland.

Ingrid Keller, MSc, MPH
Associate Professional Officer, ALC,
World Health Organization,
Geneva, Switzerland.


Introduction
Within the next few decades, one of the defining features of the world population will be the rapid increase in the absolute and relative numbers of older people in both developing and developed countries. We are currently at the threshold of global aging. Worldwide, the total number of older people--defined as those over 60 years of age--is expected to increase from 605 million in 2000, to 1.2 billion by the year 2025.1 Currently, approximately 60% of older persons live in the developing world, a number that is expected to increase to 75% (840 million) by the year 2025. Figure 1 shows the proportional increase of older persons among the total population for some developing countries as compared to the Canadian population.

In the year 2000, in a number of developed countries, there were, for the first time, more people aged 60 and older than there were children under the age of 14.1 Population aging could be compared with a silent revolution that will impact on all aspects of society. It is imperative that we are adequately prepared for it: the opportunities and the challenges are multiple.

Cancer and Aging: Two Sides of the RecQ-Like Helicase Coin

Cancer and Aging: Two Sides of the RecQ-Like Helicase Coin

Teaser: 

Haim Cohen, Ph.D
Department of Pathology,
Harvard Medical School,
Boston, MA

The incidence of cancer increases as we age: during the last decade of life, the risk of developing cancer is a startling 50% for men and 33% for women.1 What is the underlying link between aging and cancer? This link may be found by investigating diseases that are associated with both a high frequency of cancer and premature signs of aging. Such diseases, known collectively as RecQ syndromes, are caused by mutations in genes encoding RecQ-like proteins.2 The RecQ family of proteins has a high degree of homology to the helicase domain of the RecQ helicase of E. coli. The helicase region is required for all RecQ helicases to unwind duplex DNA from 3' to 5' direction in vitro; however, the in vivo function of the eukaryotic RecQ is unknown.

At least three inherited human diseases are caused by mutations in RecQ-like genes: Werner syndrome (WS), Bloom syndrome (BS), and Rothmund-Thomson syndrome (RTS).3 These diseases share two main features: premature aging and a high level of genomic instability that manifests itself as a high incidence of cancer.

The hallmark of Bloom syndrome is an increased level of sister chromatid exchange, and patients present with sun-sensitive skin pigmentation and a predisposition to certain malignancies.

Use it or Lose it! Is Weakening Musculature a Result of Aging or Muscle Disuse?

Use it or Lose it! Is Weakening Musculature a Result of Aging or Muscle Disuse?

Teaser: 

Nadège Chéry, PhD

If physical appearance owes its beauty to strong, shapely muscles, it is a rather short-lived feature of human charm, as nice biceps, sculpted thighs and other graceful or bulging aspects of our musculature eventually wither as we age. Far more than our attractive physique is altered, unfortunately, since with advancing age the loss of muscle strength and mass also greatly contributes to frailty (resulting in falls and fractures).1 Nevertheless, this undeniable consequence of the aging process is not entirely unavoidable. Indeed, simple, effective strategies that can significantly slow (or perhaps reverse) the age-related decline in muscular performance exist, yet they are often overlooked (or even feared) by the elderly.

In an individual between 30 and 80 years of age, muscle, the largest tissue of the human body,1 undergoes important decreases (up to 40%) in both strength and mass.10 This age-related loss of muscle strength and mass is typically referred to as "sarcopenia".3,9,10 The expression "muscle wasting" is also used in geriatric medicine in reference to unintentional loss of weight, when fat mass and fat-free mass decrease, as occurs following starvation (at any age) or in geriatric failure to thrive.7,8

The extent of the loss of strength is not the same across different types of muscles, and also varies greatly among individuals.

Aging: The Dance of a Few Genes

Aging: The Dance of a Few Genes

Teaser: 

 

Anna Liachenko, BSc, MSc
Managing Editor,
Geriatrics & Aging

A number of groundbreaking studies seem to suggest that only a few genes are responsible for the multiple changes in our bodies, which lead to the gradual physiological decline, we call aging. The small number of genes involved in aging supports a thesis that was first proposed by Dr. George Martin of the University of Washington.

Using a new technology called oligonucleotide microarrays (or gene chips), to detect the rates of gene transcription, Dr. Richard A. Lerner together with Dr. Peter G. Schultz and other colleagues, recently examined 6000 genes expressed in human fibroblasts from both young and aging humans. They found that only 61 genes consistently showed changes in levels of expression with aging. More than half of these genes were involved in either cell cycle progression or remodeling of extracellular matrix. These cellular markers of aging may be fibro-blast-specific or at least mitotically-active-tissue specific as they are different from those found in post-mitotic tissues. Indeed, Dr. Tomas A. Prolla, who examined transcription rates in post-mitotic mouse gastrocnemius muscle, found a different (but, interestingly, just as narrow) subset of genes, for which the transcription rates were significantly altered with age.

In light of the small number of genes that presumably are able to cause the decline of multiple physiological systems, it is interesting to look at a group of genetic disorders called progerias. Progeria means early aging, in Greek.

Why Do We Age? What Do Dolly’s Telomeres Tell Us?

Why Do We Age? What Do Dolly’s Telomeres Tell Us?

Teaser: 


Two Theories Linking DNA Damage and Aging: Free Radical/Oxidation vs. Telomere Shortening

Ruwaida Dhala-Vakil, BSc, MSc

There are many factors involved in human aging, and significant progress has been made in this field over the last few decades. Recent evidence from cloned calves suggests that scientists may not merely be able to reverse the cellular damage accumulating with age--they may, in fact, be able to prolong cell life. The cells from these cloned animals lived longer in culture and had longer telomeres than their normal counterparts. If this extension of the cellular life span can be translated into longer life for the entire organism, the calves may live fifty percent longer than normal.1 Additionally, studies on antioxidants show that transgenic Drosophila (the fruit fly), which overexpress antioxidant genes, live 34% longer than controls.2 This article will focus on both the free radical/oxidation theory of aging, and the role of telome-rase in aging.

Free Radical/Oxidation Theory of Aging
In 1956, Denham Harman suggested that there is an age-related accumulation of reactive oxygen species (ROS) which causes damage to cellular components. The damage is targeted to the proteins and DNA in the nucleus and mitochondria, as well as to the proteins and lipids in the cell membrane, and the proteins of the cytoplasm. Mitochondrial DNA is located near the inner mitochondrial membrane, close to the sites where free radicals form.