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How Does Someone With Alzheimer Die
A healthy human brain has tens of billions of specialized neuron cells that process and transmit information through electrical and chemical signals. They send messages between different parts of the brain, and from the brain to the muscles and organs of the body. Alzheimer’s disease disrupts this communication between neurons, resulting in loss of function and cell death.
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Neurons are a key player in the central nervous system, but other types of cells are also important for healthy brain function. In fact, glial cells are the most numerous cells in the brain, outnumbering neurons by about 10 to 1. neuron For example, microglia protect neurons from physical and chemical damage and are responsible for clearing foreign substances and cellular debris from the brain. To perform these functions, glial cells often work together with the brain’s blood vessels. Together, glial cells and blood vessels regulate the delicate balance within the brain to ensure it functions at its best.
The brain usually shrinks to some extent in healthy aging, but, surprisingly, it does not lose neurons in large numbers. In Alzheimer’s disease, however, the damage is widespread, as many neurons stop working, lose connections with other neurons, and die. Alzheimer’s disrupts important processes for neurons and their networks, including communication, metabolism and repair.
Early on, Alzheimer’s often destroys neurons and their connections in parts of the brain involved in memory, including the entorhinal cortex and hippocampus. It then affects areas in the cerebral cortex responsible for language, thinking and social behaviour. Eventually, many other areas of the brain are damaged. Over time, a person with Alzheimer’s gradually loses their ability to live and work independently. Ultimately, disease is death.
Many molecular and cellular changes occur in the brain of a person with Alzheimer’s disease. These changes can be seen in brain tissue under a microscope after death. Research is being done to determine which changes cause Alzheimer’s and which may be the result of the disease.
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The beta-amyloid protein involved in Alzheimer’s disease comes in many different molecular forms that accumulate between neurons. It results from the breakdown of a larger protein called amyloid precursor protein. One form, beta-amyloid 42, is thought to be particularly toxic. In the Alzheimer’s brain, abnormal levels of this natural protein build up and form plaques that build up between neurons and disrupt cell function. Research continues to better understand how, and at what stage of the disease, different types of beta-amyloid affect Alzheimer’s disease.
Neurofibrils are abnormal aggregates of a protein called tau that accumulate inside neurons. Healthy neurons are supported internally by structures called microtubules, which help transport nutrients and molecules from the cell body to axons and dendrites. In healthy neurons, tau normally binds to and stabilizes microtubules. In Alzheimer’s disease, however, abnormal chemical changes cause tau to detach from microtubules and attach to other tau molecules, forming strands that eventually fuse and form inside neurons. These compounds disrupt the neuron’s transmission system, which impairs synaptic communication between neurons.
Emerging evidence suggests that brain changes associated with Alzheimer’s disease may result from a complex interplay between abnormal tau and beta-amyloid proteins and several other factors. Abnormal tau appears to accumulate in specific areas of the brain involved in memory. Beta-amyloid builds up in plaques between neurons. When beta-amyloid levels reach a breaking point, tau spreads rapidly throughout the brain.
Research shows that chronic inflammation can be caused by the buildup of glial cells that are normally meant to help protect the brain from debris. One type of glial cell, microglia, engulfs and destroys debris and toxins in the healthy brain. In Alzheimer’s disease, microglia are unable to clear debris, debris, and protein aggregates, including beta-amyloid plaques. Researchers are trying to understand why microglia fail to perform this important function in Alzheimer’s disease.
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One of the studies is a gene called TREM2. Normally, TREM2 tells microglia cells to clear beta-amyloid plaques from the brain and helps fight inflammation in the brain. In the human brain, where this gene does not work properly, plaques form between neurons. Astrocytes—another type of glial cell—appear to help remove plaque buildup and other cellular debris left behind. These microglia and astrocytes cluster around neurons, but are unable to perform their waste-clearing function. In addition, they release chemicals that cause chronic inflammation and further damage the neurons they are meant to protect.
People with dementia rarely have the same brain changes as Alzheimer’s. Any number of vascular problems—problems that affect blood vessels, such as beta-amyloid deposits in the brain’s arteries, atherosclerosis (hardening of the arteries) and mini-strokes—may also be at play.
Vascular problems can lead to a decrease in blood and oxygen flow to the brain, as well as a breakdown of the blood-brain barrier, which normally protects the brain from harmful agents while allowing glucose and other necessary agents. In a person with Alzheimer’s, a defective blood-brain barrier prevents glucose from reaching the brain and prevents the clearance of the toxic proteins beta-amyloid and tau. This causes inflammation, which increases vascular problems in the brain. Because Alzheimer’s appears to be both a cause and a consequence of vascular problems in the brain, researchers are searching for mediators to break this complex and destructive cycle.
In Alzheimer’s disease, as neurons are injured and die throughout the brain, connections between networks of neurons can break down and many areas of the brain begin to shrink. In the final stages of Alzheimer’s, this process – called brain atrophy – is widespread, leading to severe brain loss.
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The ADEAR Center offers information and free print publications about Alzheimer’s and related dementias for families, caregivers and health professionals. ADEAR Center staff respond to telephone, e-mail and written requests and refer local and national resources.
Visit Alzheimers.gov for information and resources about Alzheimer’s and related dementias across the federal government.
This content is provided by the NIH National Institute on Aging (). Scholars and other experts review this content to ensure it is accurate and up-to-date.
If you would like to learn more about Alzheimer’s and dementia, please contact us at 1-800-438-4380, Monday-Friday, 8:30am-5:00pm. eastern time or email adear@Alzheimer. memory, thinking, learning and organization decline over time. It is the most common cause of dementia and usually affects people over the age of 65. There is no cure for Alzheimer’s disease, but certain medications and treatments can help manage symptoms temporarily.
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Alzheimer’s disease (pronounced “alz-HAI-mirs”) is a brain condition that causes a progressive decline in memory, thinking, learning, and organizational skills. It ultimately affects a person’s ability to perform basic daily activities. Alzheimer’s disease (AD) is the most common cause of dementia.
Alzheimer’s symptoms worsen over time. Researchers believe that the disease process can begin 10 years or more before the first symptoms appear. AD usually affects people over the age of 65.
Dementia describes the state of a person’s mental functioning. It is not a specific disease. It is a decline in mental function from a previous level that is severe enough to interfere with daily life.
A person with dementia has two or more of these specific difficulties, including a change or reduction in:
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Dementia is serious. In the milder stage, you may experience a slight decline in your mental function and need some help with your daily tasks. In the most severe stage, a person is completely dependent on others for help with simple daily tasks.
Dementia occurs when an infection or disease affects the parts of your brain involved in learning, memory, decision making or language. Alzheimer’s disease is the most common cause of dementia, accounting for at least two-thirds of dementia cases in people age 65 and older.
Alzheimer’s disease mainly affects people over the age of 65. The older you are, the more likely you are to develop Alzheimer’s.
Some people develop Alzheimer’s disease before the age of 65 – usually in their 40s or 50s. This is called early Alzheimer’s disease. It’s rare. Less than 10% of AD cases are early-onset.
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Alzheimer’s disease is common. It affects about 24 million people worldwide. One in 10 people over 65 and about a third of people over 85 have the condition.
Alzheimer’s organizations and health care providers use different terms to describe the stages of Alzheimer’s disease based on symptoms.
While conditions vary, the stages all follow the same pattern – AD symptoms progress over time.
However, no two people experience AD ​​the same way. Each person with Alzheimer’s disease will progress through the stages at different rates. Not all changes will happen to every person. Sometimes it can be difficult for providers to place someone with AD in a specific stage because the stages can overlap.
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