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- 1 What Part Of The Brain Is Affected By Cerebral Palsy
What Part Of The Brain Is Affected By Cerebral Palsy
A healthy human brain contains tens of billions of neurons, which are specialized cells that process and transmit information through electrical and chemical signals. These cells send messages between different parts of the brain, and from the brain to muscles and organs. Alzheimer’s disease disrupts this communication, causing a complete loss of brain function as many neurons stop working properly and eventually die.
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Neurons are the main building blocks of the central nervous system, but other types of cells are also key to keeping the brain functioning properly. In fact, glial cells – a type of brain cell that provides physical and chemical support to neurons – are the largest cells in the brain. Glial cells come in different types such as microglia, astrocytes, and oligodendrocytes.
Microglia protect neurons from physical and chemical damage and are responsible for clearing foreign substances and cellular debris from the brain. Astrocytes are star-shaped glial cells with important metabolic, structural, regulatory and protective functions. Oligodendrocytes form the myelin sheath, a protective cellular coating around axons, which are long, thin cells that send electrical signals to other parts of the body.
To perform these functions, glial cells connect blood vessels to the brain. Microglial cells and astrocytes are also involved in the immune response in the brain. Together, glial cells and blood vessels regulate the delicate balance within the brain to ensure optimal function. In recent years, an increasing amount of scientific evidence suggests that the activation of microglial and astroglia cells may contribute to brain inflammation.
Brains usually shrink to some degree in healthy aging, but surprisingly, neurons don’t lose large numbers. In Alzheimer’s, however, the damage is widespread, where many neurons stop working properly, lose connections with other neurons, and eventually die. Alzheimer’s disrupts important processes in neurons and their networks, including communication, metabolism, and repair.
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Initially, Alzheimer’s often destroys the connections between neurons in the parts of the brain involved in memory, including the entorhinal cortex and the hippocampus. It then affects the area of the brain that is responsible for language, reasoning and social behavior. Finally, many other parts of the brain and surrounding nerves are damaged and stop working properly. Over time, a person with Alzheimer’s gradually loses their ability to live and function independently. Finally, the disease is fatal.
Before the early 2000s, the only way to tell if someone had Alzheimer’s or another form of dementia was by looking at molecular and cellular changes in the brain under a microscope after death. Thanks to advances in research, diagnostic tests including brain PET scan imaging and blood tests are now available to help doctors and researchers identify biomarkers related to dementia in the living person, making the diagnosis more accurate and more accurate. first. Research is being done to identify changes that may cause Alzheimer’s disease and which may be the cause of the disease.
The beta-amyloid protein involved in Alzheimer’s is produced by the breakdown of a larger protein called amyloid precursor. It comes in the form of different molecules that accumulate between neurons. Beta-amyloid 42 is thought to be toxic. In the Alzheimer’s brain, different levels of this normal protein clump together to form plaques that disrupt cell function.
Research is changing to better understand how, and during the course of the disease, different types of beta-amyloid affect Alzheimer’s. In July 2023, the US Food and Drug Administration granted its first traditional approval of the anti-amyloid drug lecanemab for its ability to reduce amyloid plaques and slow the progression of cognitive decline associated with Alzheimer’s. Learn more about lecanemab and other drugs and other treatments for Alzheimer’s.
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Neurofibrillary tangles are abnormal clumps of protein called tau that collect inside neurons. Healthy neurons are supported on the inside by structures called microtubules, which help guide nutrients and molecules from the cell body to the axon and dendrites. In healthy neurons, tau often binds and stabilizes microtubules. In Alzheimer’s disease, however, abnormal chemical changes cause tau to detach from microtubules and stick to other molecules, forming fibers that eventually join together to form tangles. ‘into neurons. These tangles interfere with the movement of neurons, which disrupts synaptic communication between neurons.
Emerging evidence suggests that Alzheimer’s-related brain changes may result from a complex interaction between tau protein and abnormal beta-amyloid and many other factors. It appears that abnormal tau accumulates in certain areas of the brain involved in memory. Beta-amyloid accumulates in plaques between neurons. As beta-amyloid levels reach a peak, there is a rapid spread of tau in the brain.
In Alzheimer’s, as neurons are injured and stop working properly throughout the brain, the connection between the network of neurons can break down, and many areas of the brain begin to weaken. With the final stages of Alzheimer’s, this process – called brain atrophy – is widespread, resulting from significant cell death that causes the loss of brain tissue.
Research shows that chronic inflammation can be caused by an increase in harmful secretions of dysfunctional glial cells. Healthy glial cells help keep the brain healthy. A type of glial cell called microglia engulfs and destroys waste and toxins in the healthy brain. When microglia fail to clear debris, debris, and protein aggregates, including beta-amyloid plaques, Alzheimer’s can develop. Researchers are trying to figure out how and why microglia work.
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One study focuses on a protein called TREM2, which is important for proper microglial function during stressful events, including neurodegenerative diseases. When TREM2 doesn’t work properly, plaques form between neurons. Astrocytes – another type of glial cell – help clear the accumulation of plaques and other debris. Microglia and astrocytes are misaligned and collect around neurons but do not perform their waste-clearing function. They can release chemicals that cause chronic inflammation and damage the neurons they are meant to protect.
Depressed people sometimes experience several vascular problems at the same time – problems that affect blood vessels, such as beta-amyloid deposits in the brain, atherosclerosis (hardening of the arteries), and mini-strokes – a combination which can negatively affect the brain health. Cardiovascular problems such as high blood pressure, diabetes, and stroke can damage blood vessels and reduce oxygen and nutrients to the brain, causing complex damage and a greater chance of vascular defects.
Neurological problems can lead to a decrease in blood and oxygen to the brain, as well as a breakdown of the blood-brain barrier, which often prevents harmful substances from entering the brain and allows glucose and other important molecules to pass through. In someone with Alzheimer’s disease, disruption of special transport proteins in the blood brain barrier can prevent glucose from reaching the brain and prevent beta-amyloid and toxic proteins from being cleared. This leads to inflammation, which can worsen pathological changes in the brain. A recent study showed a link between glucose metabolism in the brain and many aspects of Alzheimer’s, including gender differences in the risk and severity of the disease. Researchers continue to explore potential mechanisms to disrupt this complex and destructive process.
Scientists continue to elucidate the complex molecular and cellular changes associated with Alzheimer’s and how they lead to the characteristic features of the disease. Because these changes initially affect the parts of the brain that are important for creating new memories, memory problems are one of the first signs of cognitive impairment related to Alzheimer’s. Over time, other parts of the brain become involved, causing worsening problems with thinking, thinking, and remembering. At the end of the disease, the brain damage is so extensive that the person can no longer communicate and is dependent on others for care.
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The ADEAR Center provides free information and publications about Alzheimer’s disease and dementia for families, caregivers and health professionals. ADEAR Center staff answer phone, email, and text requests and refer to local and national resources.
Explore the Alzheimers.gov website for information and resources about Alzheimer’s and related dementias from across the federal government.
This content was provided by the NIH National Institute on Aging (). This content is reviewed by scientists and other experts to ensure that it is accurate and up-to-date. Anxiety occurs when a part of the brain, the amygdala, detects a problem. When he sees a threat, real or imagined, he uses hormones (including cortisol, the stress hormone) and adrenaline to make the body stronger, faster and stronger. This is the fight or flight response and it has kept us alive for thousands of years. It’s a tough, healthy thing to do.
Children with anxiety disorders often have anxiety disorders (GAD), phobias, or obsessive compulsive disorder (OCD). These conditions used to be thought of as “adult” illnesses, but mental health workers are finding that they are increasing in children under the age of eighteen.
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