Alzheimer’s disease (AD) is a progressive neurodegenerative disorder defined by a decline in cognitive functions like memory and thinking. The disease is not confined to the brain’s memory centers; its neuropathology eventually extends to regions that control movement, leading to significant motor impairments. These physical changes manifest as problems with coordination, mobility, and muscle integrity, profoundly affecting independence and quality of life.
The Central Nervous System and Motor Control Breakdown
The physical decline associated with Alzheimer’s disease begins not in the muscles themselves, but in the brain’s command centers. The characteristic pathology of AD, involving the accumulation of beta-amyloid plaques and neurofibrillary tangles of tau protein, damages neurons beyond the hippocampus. This cellular destruction spreads to areas responsible for initiating and executing movement, including the motor cortex, the basal ganglia, and the cerebellum.
The damage interrupts the signals that travel from the brain down to the spinal cord and ultimately to the muscles. This signal transmission failure means the muscles do not receive clear instructions for movement, even if the muscle tissue is initially healthy. The severity of motor dysfunction is associated with the burden of tau tangles, especially in the sensorimotor and frontoparietal regions of the cortex, which are responsible for planning, coordinating, and executing complex movements.
When the signal pathway is compromised, the brain struggles to coordinate the sequential firing of muscle groups needed for fluid motion. This failure leads to higher-order motor dysfunction. The resulting poor muscular response and lack of coordination are direct consequences of the brain’s inability to issue a clear motor command.
Manifestations of Physical Decline
The breakdown in central motor control leads to several physical symptoms that affect daily mobility. Gait disturbances are a common early manifestation, characterized by a slower walking speed, reduced stride length, and an increase in stride-to-stride variability. Patients often adopt a “cautious gait” as they attempt to compensate for poor balance and instability.
As the disease advances, extrapyramidal signs become more evident, resembling symptoms seen in Parkinsonism. These include bradykinesia, which is a slowing of movement, and muscle rigidity. Postural instability also increases, frequently resulting in a stooped posture and a reduction in the natural arm swing that provides momentum during walking.
A major consequence of this motor command failure is apraxia, a difficulty performing purposeful, complex motor tasks despite having the physical strength to do so. This high-level coordination loss affects routine activities like dressing, using utensils, or manipulating objects, as the brain cannot properly sequence the required muscle movements. These cumulative issues contribute to a risk of falling that is more than double that of cognitively healthy older adults, often leading to severe injury and further functional decline.
Systemic Effects and Secondary Muscle Loss
Beyond the direct neurological effects, Alzheimer’s disease leads to systemic changes that compromise the muscular system’s integrity. Sarcopenia, defined as the loss of skeletal muscle mass and function, is accelerated in AD patients, driven largely by reduced physical activity and mobility. The motor and cognitive deficits cause patients to move less, leading to disuse atrophy that is more severe than in individuals with sarcopenia who are cognitively intact.
This muscle wasting is compounded by severe dysphagia, or difficulty swallowing, which is highly prevalent in moderate to severe AD, affecting up to 93% of patients. Dysphagia results from the cortical breakdown of the complex muscular coordination required for safe swallowing, which can manifest as swallowing apraxia. This impairment drastically reduces food and liquid intake, causing weight loss and malnutrition, and increases the risk of aspirating food or liquid into the lungs.
Aspiration pneumonia is the leading cause of death in end-stage AD. Furthermore, the immobility that characterizes late-stage AD leads to the development of joint contractures. These are permanent shortenings of the muscles, tendons, and connective tissues around joints. Contractures are a direct result of prolonged positioning and lack of movement, further limiting range of motion and complicating hygiene and care.
Managing Physical Impairments
Interventions focused on maintaining mobility and function are important for slowing the physical decline in Alzheimer’s disease. Physical therapy (PT) plays a primary role, focusing on exercises to preserve muscle strength, improve balance, and maintain the range of motion required for walking. Early PT intervention has been shown to be associated with improvements in gait and balance, which can delay further functional deterioration.
Occupational therapy (OT) works to maximize independence by adapting the individual’s environment and daily tasks to their changing abilities. This includes simplifying complex routines, suggesting adaptive equipment, and modifying the home environment to compensate for coordination losses and visual-spatial deficits. OT strategies are especially helpful in managing apraxia and ensuring safety during activities like dressing and feeding.
Consistent, supervised exercise is an important component in combating disuse atrophy and the progression of sarcopenia. Low-impact activities such as walking, stretching, and Tai Chi help to maintain cardiovascular health and lower body strength. Environmental safety modifications, such as removing clutter and loose rugs, installing grab bars, and ensuring adequate lighting, are also necessary to mitigate the significant fall risk associated with the disease.