An Innovative Framework for Integrative Rehabilitation in Dementia

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with multiple pathophysiological mechanisms affecting every organ and system in the body. Cerebral hypoperfusion, hypoxia, mitochondrial failure, abnormal protein deposition, multiple neurotransmitters and synaptic failures, white matter lesions, and inflammation, along with sensory-motor system dysfunctions, hypodynamia, sarcopenia, muscle spasticity, muscle hypoxia, digestive problems, weight loss, and immune system alterations. Rehabilitation of AD patients is an emerging concept aimed at achieving optimum levels of physical and psychological functioning in the presence of aging, neurodegenerative processes, and progression of chronic medical illnesses. We hypothesize that the simultaneous implementation of multiple rehabilitation modalities can delay the progression of mild into moderate dementia. This chapter highlights recent research related to a novel treatment model aimed at modifying the natural course of AD and delaying cognitive decline for medically ill community-dwelling patients with dementia. For practical implementation of rehabilitation in AD, the standardized treatment protocols are warranted

Implication of Integrative Treatment Strategies for Real-Life Geriatric Patients with Multiple, Chronic Illnesses: A 60-Month Follow-Up of a Naturalistic Study

Neurodegeneration [Stroke and Alzheimer disease (AD)] is fastly becoming one of the leading causes of age-associated disability, dementia, and death. In addition, the Centers for Disease Control and Prevention (CDC) and the National Center for Health Statistics recently reported that AD has surpassed diabetes as a leading cause of death and is now considered the sixth-leading cause of death in the United States. Unfortunately, currently no effective treatments are available against this devastating disease. In the past we have shown the preservation and improvement of cognitive tasks in depressed and demented patients after 24 and 36 months of combined pharmacological and non- pharmacological treatment. Here we present the results of our ongoing, naturalistic study, in the same outpatient setting, at the 60 month follow up. The study group consisted of 156 medically ill, physically-disabled patients with mild to moderate dementia and depression. Patients were treated with antidepressants, cholinesterase inhibitors, and NMDA antagonists, along with their regular medication regimen. Non-pharmacological intervention was centered on a home-based program of physical and cognitive exercises as well as with vitamins and supplements (multivitamins, vitamin E, L-methylfolate, alpha-lipoic acid, acetyl-l-carnitine, omega-3, and coenzyme Q-10) and diet modification. Cognitive assessments were performed yearly. After 60 months of treatment, performance of all tasks remained at or above baseline. The MMSE, Cognistat–Attention, Cognistat–Judgment, and RFFT - Total Unique Designs demonstrated significant improvement. Our results, for the first time, demonstrate arrest in cognitive decline in demented/depressed patients with multiple medical co-morbidities for 60 months. Future investigations addressing the application of a combined, integrative treatment models in clinical practices are warranted

Oxidative Stress Induced Mitochondrial Failure and Vascular Hypoperfusion as a Key Initiator for the Development of Alzheimer Disease

Mitochondrial dysfunction may be a principal underlying event in aging, including age-associated brain degeneration. Mitochondria provide energy for basic metabolic processes. Their decay with age impairs cellular metabolism and leads to a decline of cellular function. Alzheimer disease (AD) and cerebrovascular accidents (CVAs) are two leading causes of age-related dementia. Increasing evidence strongly supports the theory that oxidative stress, largely due to reactive oxygen species (ROS), induces mitochondrial damage, which arises from chronic hypoperfusion and is primarily responsible for the pathogenesis that underlies both disease processes. Mitochondrial membrane potential, respiratory control ratios and cellular oxygen consumption decline with age and correlate with increased oxidant production. The sustained hypoperfusion and oxidative stress in brain tissues can stimulate the expression of nitric oxide synthases (NOSs) and brain endothelium probably increase the accumulation of oxidative stress products, which therefore contributes to blood brain barrier (BBB) breakdown and brain parenchymal cell damage. Determining the mechanisms behind these imbalances may provide crucial information in the development of new, more effective therapies for stroke and AD patients in the near future