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Unlike the degenerative disorders that cause dementias, which stem from a modest number of aberrant processes, aging-related cognitive changes reflect a host of mechanisms. These include mechanisms associated with a person’s condition, e.g., drugs, pain, depression, and sleep disorders. They include mechanistic changes linked to the aging process, e.g., enhanced neural network noise, increased neighborhood density, age of acquisition effects, degraded selective engagement of neural networks, alteration of the balance between volitional and reactive intention and attention, declines in neurotransmitter function, and brain ontogenesis over the life span. They include changes best characterized as senescent physiology and best demonstrated in decline in functions essential to episodic memory formation related to impaired encoding in the hippocampal cornu amonis (CA) fields and slowed neurogenesis in the hippocampal dentate gyrus. Finally, they include processes best characterized as senescent pathology, the best understood being degradation of myelin and associated reduction of central conduction velocities and slowing of processing speed. No longer should cognitive changes associated with aging be viewed as a simple manifestation of a unitary aging process. The large number of mechanisms at play and their complexity offer many opportunities for therapeutic intervention.
Our brains are continuously changing and these changes alter brain functions. With maturation, there is growth and unfortunately, even with healthy aging, decline. Aging-related decrements affect neurons and their connectivity, neurotransmitter systems, and even support systems such as glia. Aging affects some brain regions (frontal lobes and hippocampi) more than others. This book reviews and discusses aging-related changes and their influence on the major neurobehavioral domains, beginning with reviews of aging-related changes in anatomy and physiology. Subsequent chapters review cross-sectional and longitudinal studies of aging-related changes in sensory perception (vision, hearing, touch, smell, taste) and cognitive functions (memory, language, motor planning, attention, executive functions, emotions, creativity). In each chapter, mechanisms that may account for these changes are discussed. Declines related to aging per se are distinguished from declines related to aging-associated diseases. Final chapters discuss what can potentially be done to slow or reverse aging-related decline of cognitive functions, including exercise, cognitive rehabilitation, and pharmacological agents. It is hoped this book will help clinicians differentiate between normal aging processes and brain diseases, reduce the adverse effects of brain aging, and stimulate further research on how adverse effects of brain aging can be reversed, stopped, modified, or best managed.
Aging is associated with decline in a number of domains of language function, most conspicuously lexical-semantic function (manifesting as word-finding difficulty), but also semantics, phonological sequence, grammatic morphology, language comprehension, syntax (so far linked only to working memory deficits), and narrative discourse. There is evidence of a number of non-disease-related mechanisms that could account for this, including increased neural network noise, age of acquisition effects, deterioration of mechanisms of selective neural network engagement, deterioration in episodic memory, alteration of the balance between volitional and reactive intention, lifelong ontogenesis of language networks, and reduction of white matter conduction velocities.
This book describes the changes in the brain and in cognitive functions that occur with aging in the absence of a neurological, psychiatric, or medical disease. It discusses aging-related changes in many brain functions, including memory, language, sensory perception, motor function, creativity, attention, executive functions, emotions and mood. The neural mechanisms that may account for specific aging-related changes in cognition, perception and behavior are explored, as well as the means by which aging-related cognitive decrements can be managed and possibly ameliorated. Consequently, this book will be of value to clinicians, including neurologists, psychiatrists, geriatricians, primary care physicians, psychologists and speech-language pathologists. In addition, researchers and graduate students who want to learn about the aging brain will find this an indispensable guide.
Six individuals with probable Alzheimer’s disease (AD) participated in a phase 1 study employing a repeated measures, parallel baseline design testing the hypothesis that error-free experience during word production practice combined with an acetyl cholinesterase inhibitor would improve confrontation naming ability. While acetyl cholinesterase inhibitors are safe and delay cognition decline associated with AD, improvement over baseline cognition is less evident; clinically significant cognitive deficits persist and progress. Both animal and clinical research strongly implicate acetylcholine in learning, a form of neuroplasticity. In clinical practice, however, people with AD are given cholinergic medications without concomitant systematic/targeted retraining. In this study six participants with probable AD and taking donepezil participated in targeted word production practice using an errorless learning strategy. Results showed that combining behavioral enrichment training and an acetyl cholinesterase inhibitor resulted in significant improvements in verbal confrontation naming of trained items for three of six participants. Differences in baseline dementia severity, living conditions, and medications may have influenced the training response. Detection of substantial treatment effects in 50% of subjects suggests further language treatment studies in AD in combination with an acetyl cholinesterase inhibitor are warranted and provide useful information on inclusion/exclusion criteria for use in subsequent studies. (JINS, 2009, 15, 311–322.)
In this issue of JINS, Gasparini and her colleagues (2008) report a subject with a right anterior choroidal artery territory stroke that damaged the anterior hippocampus, but likely more importantly, much of the ventral posterior limb of the internal capsule, effectively disconnecting the right thalamus from temporal cortex. Through systematic cognitive neuropsychological detective work, they provide a compelling case that the essential deficit was one of working memory. This is potentially a very important discovery. The thalamus is a phylogenetically ancient structure, and there is considerable evidence that, in human beings, much of its function has been subsumed by cortical mechanisms (Nadeau & Crosson, 1997). Consequently, there are fundamental limits to how much animal studies can inform us about human thalamic functions, and we are particularly reliant on cognitive neuropsychological studies like this one. The work of Gasparini et al. also provides a fine demonstration of the continuing value of cognitive neuropsychology in advancing our understanding of the details of brain function.
Rapid innovations and improvements in communication technologies have opened many new channels for health education and delivery, as well as disaster management. Theme 2 examined the role and applicability of these technologies to Disaster Medicine and Management and the various issues involved in their use.
Details of the methods used are provided in the introductory paper. The chairs moderated all presentations and produced a summary that was presented to an assembly of all of the delegates. The chairs then presided over a workshop that resulted in the generation of a set Action Plans that then were reported to the collective group of all delegates.
Main points developed during the presentations and discussion included harnessing convergence, seeking interoperability, building partnerships and making it appropriate. This group identified four Principles of Action underlying its plan: (1) investigate possibilities, (2) identify stake-holders, (3) invite participation, and (4) involve discussants in activities.
Action plans were categorized into three areas that included “thinking globally, acting regionally”, forming a telehealth advisory group, and increasing corporate partnerships.
Technology is opening many opportunities that have applications in disaster management. To optimize benefits, goals and standards must be agreed upon and implemented.
Patients with probable Alzheimer's disease
(AD) often have difficulties associated with semantic knowledge.
Therefore, conceptual apraxia, a defect of action semantics
and mechanical knowledge, may be an early sign of this
disease. The Florida Action Recall Test (FLART), developed
to assess conceptual apraxia, consists of 45 line drawings
of objects or scenes. The subject must imagine the proper
tool to apply to each pictured object or scene and then
pantomime its use. Twelve participants with Alzheimer's
disease (NINCDS–ADRDA criteria) and 21 age- and education-matched
controls were tested. Nine Alzheimer's disease participants
scored below a 2-standarddeviation cutoff on conceptual
accuracy, and the three who scored above the cutoff were
beyond a 2-standard-deviation cutoff on completion time.
The FLART appears to be a sensitive measure of conceptual
apraxia in the early stages of Alzheimer's disease.
(JINS, 2000, 6, 265–270.)
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