Pathophysiology of Alzheimer’s Disease
The core pathological findings in Alzheimer’s disease include extracellular amyloid
plaques, intracellular neurofibrillary tangles and neuronal degeneration. Amyloid plaques are a
cardinal feature of AD. They are complex structures which consist of a core of A amyloid
protein and surrounded by dystrophic dendritic processes (Serrano-Pozo, Frosch et al., 2011)
which are deposited in the cortex. This leads to neuronal damage of the medial temporal lobe
structures and the frontal cortex, consisting of the hippocampus. In the normal brain, the
protein fragments are usually eliminated. But in Alzheimer’s disease the fragments harden to
form plaques and accumulate in the brain. The
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These are intraneuronal aggregates of insoluble cytoskeletal protein,
formed from hyperphosphorylation of tau protein. Since the tau protein is abnormal in AD, the
microtubular functions are impaired. The other additional changes we can witness in the AD
brain include cerebral amyloid angiopathy, synaptic loss, Hirano body formation and
granuovacuolar degeneration (Perl D, 2010). Alzheimer’s disease is a slowly progressive disease
in which these lesions develop over many years and eventually lead to functional impairment.
(Parl, Lee et al., 2012). As a result of the changes in the brain, Alzheimer’s patients begin with a
decline in short term memory. Followed by alterations in mood and personality, progressive
disorientation, language dysfunction and apraxia. This causes the inability of the patient to care
for himself/herself and eventually causes them to be bedridden.
Genetics of Early vs Late of Alzheimer’s Disease
Early onset Alzheimer’s disease is usually seen among people 65 years and younger. It
accounts for about 6-7% of the cases (Ridge, Ebbert et al., 2013) of AD. Mutations in three
different genes are known to be the causal factor for Early onset AD. These genes
Percy, A. K. (1999). Inherited neurodegenerative disease: The evolution of our thinking. Journal of Child Neurology, 14(4), 256-62. Retrieved from
This is a disease is found in the brain and is caused by a buildup of a protein called tau. Tau slowly kills brain cells. Even after brain trauma has ended this process still continues. There are many symptoms such as memory loss, confusion, impaired judgement, depression, and even aggression.
Attention Deficit Hyperactivity Disorder (ADHD) is a developmental disorder that displays as distracted, hyperactive, and unable to focus on tasks and activities. Also known as Hyperkinetic Impulse Disorder, Hyperkinesis, Hyperactive Syndrome, Minimal Brain Damage, Minimal Brain Dysfunction, and Undifferentiated Deficit Disorder, ADHD is the most commonly diagnosed neurological disorder in children. Although many children with ADHD are quite intelligent, their lack of focus can frequently lead to poor grades and a low self esteem. The exact cause of ADHD is still unknown, but it is considered highly inheritable. Results from numerous international studies on twins have found that ADHD may have a genetic link. The occurrence of ADHD in one twin is more often mirrored an identical twin who has the same genetic makeup, then in a fraternal twin whose genetics are similar but not identical. It is also believed that if a parent, uncle, or grandparent had ADHD, it is more likely their family may develop it as well. No gene has been discovered that directly relates to the disorder. MRI studies comparing the brains of children with and without the condition have shown that children with ADHD have weaker brain activity in the frontal area of the brain when responding to tasks that require inhibition. Because of this, it is thought that ADHD affects certain sections of the frontal cortex, parietal lobe, and possibly parts of the cerebellum.
Clinically, Alzheimer’s disease is characterized by the accumulation of beta-amyloid plaque between living neurons in the brain (Sabbagh, 2008). This results in an excessive calcium influx inside the neurons and the breakdown of a protein called tau. Normally, the rol...
There are seven stages of Alzheimer’s, classified by Dr. Barry Reisberg, M.D. clinical director of the New York University School of Medicine’s Silberstein Aging and Dementia Research Center. Each stage carr...
of diagnosis is about 80 years old (Johnson, 1989). The incidence is about the same for all races, but women are more likely than men to develop the disease, because they live longer. The second factor is heredity. Family history plays a role in about forty percent of people with early onset of Alzheimer’s (Johnson, 1989). If your parents or a sibling developed the disease, you are more likely to, as well. But there are cases of families with several people who have had this disease and other members are not affected. These two factors are the only proven factors, but environmental research is being done to help with a possible protective effect for the disease. As of now, more research is needed to confirm any be...
There are definitely people with a genetic vulnerability. However, there are also others with biological vulnerabilities. ADHD is a real disorder with implications to problems with brain chemistry and function. It is also know to be one the most commonly diagnosed disorders in school aged children. Today we use brain scan studies and genetic studies to help us diagnose this disorder. However, we have learned that is a heterogenous disorder and is still a very low-tech diagnosis based on symptoms (Ullman,
Since the gene for HD is dominant, there is a 50% chance of a sufferer's
Chronic Traumatic Encephalopathy, also known as CTE, is a neurodegenerative disease where an excess amount of tau, an abnormal protein, builds up inside of the brain. According to “A critical review of chronic traumatic encephalopathy”, the disease also creates “multiple blockages of the axonal transport to the brain cells, along with white spaces in the brain on a MRI scan.”, as
how it is born. Initially when we study the brain of a Alzheimer's victim, we
Scientists believe that for most people, Alzheimer's results from a combination of genetics, lifestyle and environmental factors that affect the brain over time. Alzheimer's is caused by specific genetic changes that virtually guarantee a person will develop the disease. The causal effect for this disease is still unknown with fingers pointing to plaques and tangles in the brain. Although the causes of Alzheimer's are not yet fully understood, its effect on the brain is clear. Alzheimer's disease damages and kills brain cells. A brain affected by Alzheimer's disease has many fewer cells and many fewer connections among surviving cells than does a healthy brain. As more and more brain cells die, Alzheimer's leads to enormous brain shrinkage. When doctors examined an Alzheimer's brain tissue under the microscope, they saw two types of abnormalities that are considered the cause of the disease. One of these abnormalities is plaques that clump up, a protein called beta-amyloid which damages and destroys brain cells. In patients with Alzheimer’s the plaques created interfere with cell to cell communication. The other abnormality seen is tangles in the brain. Brain cells depend on an internal support and transport system to carry nutrients and other essential materials throughout their long extensions. This system requires the normal structure and functioning of a protein called tau. In an Alzheimer's patient, the threads of tau protein twist into abnormal tangles inside the brain cells, leading to failure of the transport system. (Alzheimer's Association) (National Institutes of Health, 2012)
“Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve cells, or neurons, resulting in loss of memory, thinking and language skills, and behavioral changes” (Alzheimer’s Foundation of America, 2014). AD is a debilitating disease that interferes with the individual’s quality of life and often causes distress to the loved ones around them. The cause of AD is unknown; however, there are some factors that put individuals at risk for developing AD such as: age (gre...
Alzheimer’s disease (AD) is a progressive, terminal, degenerative brain disease. It is the fourth leading cause of death in adults and currently affects over four million people in the United States. This number is expected to increase over the next several years as the baby boomers age, until it reaches fourteen million by the year 2025.
Biology The brain consists of both neurons and glia cells. The neurons, which are cells housed in a cell body called a Soma, have branches which extend from them, referred to as dendrites. From these dendrites extend axons which send and receive impulses, ending at junction points called synapses. It is at these synapse points that the transfer of information takes place. At the heart of neuroplasticity is the idea of synaptic pruning.
Because A"β" is critical to the pathogenesis of Alzheimer’s disease, “it is imperative to understand the molecular and cellular basis of its production” (Bali 2010). The A"β" peptides themselves are formed from an Amyloid Precursor Protein, “ by the sequential action of of "β" - sycretase and "γ " secretase” and are released, forming plaques. The toxic properties of these plaques include the phosphorylation of tau, thus the creation of tangles in the brain, and neurodegeneration (Bali 2010).