Introduction
Alzheimer’s dementia (AD) is an irreversible illness that primarily affects the brain and nervous system. It is a brain condition that gradually affects memory, cognitive abilities, and the capacity to do even the most basic activities. All mental function, including cognition, learning, and memory, is centered on the nervous system. It collaborates with the endocrine system to control and regulate body homeostasis. Alzheimer’s disease causes abnormalities in the neurological system, especially cognitive function concerns such as memory, thought process, and behavior difficulties, along with confusion and impaired judgment. In 1906, German physician Alois Alzheimer, a specialist in identifying symptoms with microscopic brain alterations, was the first to characterize the disease’s symptoms (McGirr et al., 2020). He examined Auguste Deter, a patient suffering from memory loss and disorientation. Alzheimer conducted an autopsy after her death and discovered anomalies in her brain, notably tangles and plaques that are today recognized as markers of Alzheimer’s disease.
People with mild or moderate Alzheimer’s disease have diverse but substantial cognitive, physiological, and behavioral alterations and mild-to-moderate deficits. Some early symptoms, such as mood, agitation, and sleep disturbances, emerge years before a definitive diagnosis of dementia is made. In the preclinical phases of AD, elevated levels of anxiety, depression, apathy, and disengagement are widespread (McGirr et al., 2020). Unrecognized and inadequately treated escalate to later-stage symptoms, including poor judgment, disorientation, and bewilderment; severe changes in behavior, like violence and restlessness. It can also progress to neuropsychiatric symptoms, like delusions and hallucinations, which may occur before diagnosis. Effective treatment begins with identifying early warning signs or indicators and an appropriate examination.
The incidence of dementia, mainly attributable to Alzheimer’s disease or mixed AD, is rising in America and worldwide. The number of Americans diagnosed with dementia will increase by 35% in 2030 and might even triple by 2050 (McGirr et al., 2020). In Georgia, Alzheimer’s disease is a significant public health concern. Alzheimer’s Association (2020) projects that the disease’s effect will increase, and the most current statistics indicate that 150,000 Georgians aged 65 and over are living with Alzheimer’s disease. These statistics demonstrate the need for a public health strategy to reduce the burden and improve the quality of life for persons with cognitive deficits and their families.
Normal Anatomy and Physiology of the Nervous System
A healthy brain comprises billions of neurons, unique cells that collect and transfer information through electrical and chemical impulses between various sections of the brain and the organs and muscles in the body. Neurons are essential in the central nervous system (CNS), although other cell types are equally essential for brain health. Glial cells represent the vast majority of brain cells, surpassing neurons by 10 to 1 (Fountoulakis, 2022). These cells, which include microglia, oligodendrocytes, and astrocytes, surround and maintain neurons’ good health and function. Microglia, for instance, guard neurons against chemical and physical injury and are essential for cleansing the brain of foreign chemicals and cellular debris. To perform these duties, glial cells often work with brain blood vessels. Blood vessels and glial cells collectively guarantee that the brain operates well by maintaining delicate equilibrium.
Neurons (nerve cells) that convey electrical impulses are the physiological means through which the brain gets input from the senses. The brain processes and interprets this information, culminating in a reaction such as a movement or thinking. Neurotransmitters are chemical signals released by the brain to facilitate communication between neurons and control emotion, memory, and other activities. In a non-Alzheimer’s brain, these systems are all appropriately and effectively operating, enabling normal physical and cognitive functioning.
Pathophysiology of Alzheimer’s Disease
Neuronal extracellular deposition of amyloid plaques and neuronal intracellular buildup of hyperphosphorylated tau protein to constitute neurofibrillary tangles (NFTs) are the two most prominent theories regarding the processes implicated in the pathogenesis of Alzheimer’s disease (AD) at present. However, the primary underlying cause of cognitive and behavioral deficits in Alzheimer’s disease is synapse disruption (Abubakar et al., 2022). For example, human neural dysfunction is related to a rise in A and phosphorylated tau decreases synaptic strength owing to its accumulation in the dendritic spine and subsequent import of N-methyl-d-aspartic acid receptors (NMDARs) (Abubakar et al., 2022). Other variables, such as increased oxidative stress in the aging brain, have been demonstrated to precede the development of senile plaques and the accumulation of NFTs (Abubakar et al., 2022). In addition, elevated inflammatory markers like cytokines and related genes have been linked to the onset of AD (Abubakar et al., 2022). The pathogenesis of Alzheimer’s disease is characterized by gradual brain cell death and reduced neurotransmitter concentrations, resulting in the deterioration of cognitive processes and, ultimately, dementia.
Treatment/ Prevention Options
The management of AD necessitates triadic cooperation between the physician, the client, and the caregivers. Neuropsychiatric symptoms like agitation, apathy, delusions, and problem behaviors associated with Alzheimer’s disease (AD) dementia should be treated initially with nonpharmacologic treatments and behavioral strategies (Atri, 2019). Patients and caregivers are distressed by problem behaviors, which, if left untended, exact a severe toll and result in poor results. 85% to 90% of patients will exhibit neuropsychiatric signs or behavior problems, such as behavioral and psychological symptoms of dementia (BPSD), throughout their disease (Atri, 2019). These manifestations are related to rapid deterioration, early institutionalization, anxiety, and increased healthcare consumption and expenditures. Early and continuing BPSD assessment, root-cause analysis, management, and monitoring are essential components of comprehensive Alzheimer’s disease dementia care (Atri, 2019). These early actions may improve the effectiveness of prevention and therapy by reducing triggers and targeting the underlying cause, not just the symptoms.
Psychoeducation should teach caregivers about the biopsychosocial foundations of BPSD and techniques to minimize behavioral triggers and improve patient communication and care. Caregivers must recognize that the dementia patient’s general negative and problem behavior is not deliberate but rather the result of sickness, brain damage or injury, and impaired capabilities since it is a symptom of the condition. Environmental change, regularity, and fundamental routines may also greatly assist.
In terms of pharmacological management, the first stage in the treatment of Alzheimer’s disease is the elimination of redundant and sometimes harmful drugs. For instance, diphenhydramine, which is frequently obtained as an over-the-counter drug, other hypnotics, and drugs for anxiety are contraindicated in old aged and cognitively vulnerable patients. Additionally, it is essential to detect and manage comorbid illnesses that worsen dementia. In AD patients, addressing these issues may improve cognition, functionality, and behavior. In many cases, the symptoms and indications of decompensation might be mild and persistent rather than abrupt delirium. Laboratory tests or examinations for assessing dementia may assist in detecting frequent diseases that increase symptoms, such as dehydration, anemia, electrolyte and metabolic imbalances, and heart or cerebral ischemia, among others.
Cholinesterase inhibitors (ChEIs) and memantine are two examples of FDA-approved Alzheimer’s disease treatments. Cholinesterase inhibitors (ChEIs) like rivastigmine and the N-methyl-d-aspartate (NMDA)-antagonist, memantine, are the sole FDA-approved therapies for Alzheimer’s disease dementia and are often recommended in consensus recommendations and practice norms (Atri, 2019). Memantine and ChEIs possess complementary modes of action, possibly synergistic effects, and adequate tolerance and safety profiles. Joint combination treatment, most commonly memantine added to steady baseline ChEI medication, has shown short- and long-term advantages for reducing cognitive and functional deterioration, delaying the onset and severity of neuropsychiatric symptoms.
Sustained therapy gives a moderate prospect of short-term stability or recovery and a longer-term reduction of clinical deterioration. As the condition advances, over many months to years, people who may initially exhibit recovery or stability may ultimately decline. Practitioners must discuss practical difficulties connected with pharmacologic therapy, including rationale, necessity for monitoring, and goals. In the long term, existing therapies for AD dementia minimize deterioration but do not mitigate it. Treatments that reduce caregiver load and postpone nursing home admission substantially increase worker output and reduce healthcare costs.
Conclusion
Alzheimer’s disease is a degenerative neurological ailment marked by decreased memory, speech, and other cognitive skills. Alzheimer’s disease is considered to be caused by a mix of environmental, genetic, and lifestyle factors; however, the specific etiology is unclear. Some early signs, including mood, restlessness, and sleep disturbances, appear years before a confirmed dementia diagnosis. The therapy of AD necessitates triadic cooperation between the physician, the patient, and the caregivers. Priority should be given to nonpharmacologic therapies and behavioral methods, followed by pharmacologic approaches. For these patients, it is vital to establish a comprehensive, pragmatic therapeutic partnership that incorporates psychoeducational, behavioral, and environmental strategies for treatment and planning.
References
Abubakar, M.B., Sanusi, K.O., Ugusman, A., Mohamed, W., Kamal, H., Ibrahim, N.H., Khoo, C.S. and Kumar, J. (2022). Alzheimer’s disease: An update and insights into pathophysiology. Frontiers in Aging Neuroscience, 14. Web.
Alzheimer’s Association. (2020). Alzheimer’s Disease and Dementia. Web.
Atri, A. (2019). The Alzheimer’s disease clinical spectrum. Medical Clinics of North America, 103(2), pp.263–293. Web.
Fountoulakis, K. N. (2022). Cellular structure and histological architecture of the brain. The Human Connectome, 51–59. Web.
McGirr, S., Venegas, C., & Swaminathan, A. (2020). Alzheimers disease: A brief review. Journal of Experimental Neurology, 1(3), 89-98. Web.
