Alzheimer's Disease

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1- Introduction

2- Pathophysiology

3- Symptoms

4- Treatment

Introduction

Alzheimer disease (dementia of Alzheimer type [DAT], senile disease complex) is a common neurologic disorder. Formerly believed to occur mostly in people younger than 65 years (familial, early onset dementia), AD has been demonstrated to be one of the most common causes of severe cognitive dysfunction in older adults. Its more prevalent forms are late-onset familial Alzheimer dementia (FAD) and nonhereditary, or sporadic, late-onset AD (70% of cases). FAD and sporadic, late-onset AD are known as senile dementia of the Alzheimer type (SDAT). AD is also associated with Down syndrome. It is estimated that 5 million Americans have AD.

Pathophysiology

The exact cause of AD is unknown. Several possible theories being investigated include loss of neurotransmitter stimulation by choline acetyltransferase; mutation for encoding amyloid precursor protein; alteration in apoE, which binds amyloid-beta amyloid-beta beta; and pathologic activation of N-methyl-d-aspartate (NMDA) receptors resulting in an influx of excess calcium. The pathogenesis of AD is linked to amyloid-beta (AB) pep- tide. AB peptide is derived from proteolysis of APP and released as AB 30 to AB 46, with AB 40 and AB 42 the most abundant isoforms produced. These peptides have a strong tendency to form clusters of fibrils, especially AB 42.47 A balance between production and catabolism (involving microglia, macrophages, and bulk flow across the blood-brain-barrier) is required. Altered production and failure of clearance of amyloid from the brain occur in AD initiating accumulation. Fine diffuse plaques (senile plaques) are the initial accumulation of AB 42. This accumulation is followed by other AB depositions along with tau protein, activated glia, and, eventually, neurofibrillary tangles.47 The abnormal AB is neurotoxic. Microscopically the tau protein that normally stabilizes the microtubular transport system in the neurons detaches from the microtubule and forms insoluble helical filaments called neurofibrillary tangles. Tangles are flame shaped. Cortical nerve cell processes become twisted and dilated because of accumulation of the same filaments that form tangles. Amyloid also is deposited in cerebral arteries, causing an amyloid angiopathy. Senile plaques and neurofibrillary tangles are more concentrated in the cerebral cortex and hippocampus. The greater the number of senile plaques and neurofibrillary tangles, the more dysfunction associated with AD. shows the disturbance in blood flow in AD. In addition, aging and injury may result in changes that contribute to the development of this disease. Such changes could include decreased oxygen and glucose transport, loss of the blood-brain barrier, and mitochondrial defects that alter cell metabolism and processing of proteins, including amyloid (apoE4). Macroscopically, the brain in AD decreases in volume and weight, the sulci widen, and the gyri thin, especially in the temporal and frontal lobes. The ventricles enlarge to fill the space.

Symptoms

Alzheimer’s disease is a progressive neurological disorder that primarily affects cognitive function. The symptoms typically develop slowly and worsen over time. The most common symptoms of Alzheimer’s disease include:

Memory Loss: One of the earliest and most prominent symptoms is difficulty remembering newly learned information. This can manifest as forgetting important dates or events, repeating the same questions, or relying on memory aids.
Difficulty with Problem-Solving and Planning: Individuals may experience challenges in making decisions, solving problems, or planning tasks. This can affect daily activities such as managing finances or following recipes.
Confusion and Disorientation: People with Alzheimer’s disease may become confused about time, place, or current events. They may forget where they are or how they got there, especially in unfamiliar surroundings.
Changes in Speech and Writing: Communication difficulties may arise, including problems finding the right words, following or joining a conversation, or repeating oneself. Writing may also become more challenging.
Misplacing Items: Individuals may put things in unusual places and struggle to retrace their steps to find them. This may occur more frequently over time.
Decreased Judgment: Judgment and decision-making abilities may decline, leading to poor decisions in financial matters, personal hygiene, or interactions with others.
Withdrawal from Social Activities: As cognitive function declines, individuals may withdraw from social activities, hobbies, work projects, or sports they previously enjoyed due to difficulties with memory and communication.
Changes in Mood and Personality: Alzheimer’s disease can cause mood swings, anxiety, depression, irritability, or a loss of interest in previously enjoyed activities. Personality changes, such as becoming suspicious or fearful, may also occur.
Difficulty Performing Familiar Tasks: Routine tasks that were once familiar may become challenging. This can include tasks such as dressing, bathing, cooking, or driving.
Loss of Initiative: Individuals may have difficulty initiating activities or tasks, and they may require more prompting to engage in daily activities.

Treatment

The treatment of Alzheimer’s disease aims to manage symptoms, slow disease progression, and improve the quality of life for patients. It typically involves a combination of medication, non-drug treatments, and supportive care. Here are the main approaches to treating Alzheimer’s disease:

Medications:
- Cholinesterase Inhibitors: Drugs such as donepezil, rivastigmine, and galantamine work by increasing levels of acetylcholine, a neurotransmitter involved in memory and learning. These medications can help improve cognitive symptoms and may temporarily slow down the progression of symptoms in some individuals.
- Memantine: This medication regulates the activity of glutamate, another neurotransmitter involved in brain function. Memantine is used to treat moderate to severe Alzheimer’s disease and may help improve cognitive function, behavior, and daily activities.
Non-Drug Therapies:
- Cognitive Stimulation: Activities and programs that stimulate thinking, memory, and problem-solving skills can help maintain cognitive function and delay symptom progression. These may include puzzles, memory games, and structured cognitive exercises.
- Physical Exercise: Regular physical activity has been shown to benefit overall health and may help improve cognitive function and mood in individuals with Alzheimer’s disease.
- Occupational Therapy: This can help patients find ways to manage daily activities more independently and adapt their environment to support their cognitive and functional abilities.
Supportive Care:
- Management of Behavioral Symptoms: Alzheimer’s disease can cause changes in behavior, mood swings, and agitation. Behavioral interventions, environmental modifications, and sometimes medications can help manage these symptoms.
- Nutritional Support: A healthy diet and adequate nutrition are important for overall health and well-being. Caregivers may need to assist with meal planning and ensure that patients are getting proper nutrition.
- Social Support: Engaging in social activities and maintaining relationships can provide emotional support and cognitive stimulation for patients with Alzheimer’s disease.
Clinical Trials and Research: Participating in clinical trials can provide access to experimental treatments and contribute to advancing our understanding of Alzheimer’s disease. Researchers are continually studying new medications, interventions, and strategies for treating and preventing the disease.
Caregiver Support: Alzheimer’s disease not only affects patients but also places significant demands on caregivers. Support groups, respite care, and education about the disease can help caregivers manage stress, provide effective care, and maintain their own well-being.