Alzheimer’s disease is a primary cause of death among the older adult population in the United States. It is a neurodegenerative disease of the brain that, alone, makes up 59% of all senile dementias. Today, over 5 million people in the United States have Alzheimer’s disease (AD), which includes 4.9 million people who are over the age of 65. Moreover, almost 500,000 people under the age of 65 have early onset Alzheimer’s and other types of dementia. It is estimated that a person develops Alzheimer’s disease every 72 seconds. There is currently no cure or effective treatments to slow the onset or development of AD, resulting in a prevalence that could increase to 7.7 million people by the year 2030. It is expected that by mid-century, the population of people with AD will rise to as many as 16 million.
This neurodegenerative disease causes the brain to atrophy—leading to smaller brain size and reduced gray matter. Age is a huge risk factor, with a rate of prevalence that doubles every five years after the age of 60. Family history (genetics), being female, experiencing head injury, low education, obesity, and type 2 diabetes are also major risk factors for AD.
Alzheimer’s disease involves a range of cognitive and behavioral impairments including memory loss and decreased executive function. Specifically, patients with AD can have short-term memory issues, problems in judgment and reasoning, difficulty finding words, and decreased visuo-spatial abilities. For behavior, a patient with AD may express apathy or withdrawal, have depressive mood, anxiety, and delusions.
Key components of AD neuropathology include neurofibrillary tangles, plaques, dystrophic neurites, and reactive glia. Neurofibrillary tangles are markers of dead and dying neurons of the brain. Not all dead neurons in an AD brain form neurofibrillary tangles. They are abundant in AD brains but sparse in normal aged brains and absent in those of young adults.
Plaques are the accumulation of the protein called beta-amyloid. It is thought to be the key molecule in the pathogenesis of AD. In its normal state, beta-amyloid protein are present in biological fluids in a soluble state at low levels. In AD, these beta-amyloid proteins bind together to form highly insoluble peptides and eventually become extracellular plaques.
Dystrophic neurites are another key component of AD and are associated with plaques. They are injured and dying branches of neurons in the brain. Neurites are made up of axons and dendrites that form all the connections between nerve cells, called neurons. They are very abundant in the AD brain and impair neural connections, causing the neural circuitry to be disrupted. This results in the brain unable to properly process information and impairs cognition.
Glia, which include astrocytes and microglia, are normally beneficial and function as the brain’s clean up crew, eating harmful toxins and debris that build up in the brain. When they adopt a chronically activated state, however, they may contribute to AD pathology.
As previously stated, there are currently no cures that have been found that can stop or reverse this disease’s process. There are just two classes of prescription medications that are approved to treat AD: acetylcholinesterase (Ach-E) inhibitors and NMDA receptor antagonist.
Many seniors living in nursing home facilities have Alzheimer’s disease that affects every part of their daily living. Nursing home staff and care providers must provide quality of care to meet these patients’ needs and consult with a doctor before using medication as treatment. Every older adult resident is vulnerable to adverse events when nursing home staff fail to provide quality care to their patients at all times. If you or a loved one has suffered due to inadequate care provided by a nursing home, contact us today for a free consultation.