Alzheimer's Disease

Pathophysiology Education Project | 4 Dec 2015

Sophia Amati, Alison Cargin, Olivia Pirosko, Rachel Szczepinski, Adam Clauss

What is Alzheimer's Disease?

In 1906, Dr. Alois Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. When he examined her brain, Dr. Alzheimer found abnormal clumps and tangled bundles of fibers, which are still considered the main features of the disease. Alzheimer’s disease is a degenerative neurological disease that is the main cause of dementia. It impairs memory, thinking and behavior and ultimately will negatively affect daily living. It causes gradual mental degeneration due to widespread deterioration of the brain during middle to old age. The disease is progressive, meaning the memory, thinking and behavior deficiencies worsen as time passes. The deterioration appears to start in the hippocampus and, as more neurons die, spreads to additional parts of the brain. Unfortunately, there is no current cure. Alzheimer’s is ranked in the top 5 for leading causes of death in the United States.

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The pathogenesis of Alzheimer’s Disease is typically driven by 2 processes: extracellular deposition of beta amyloid- α-βand intracellular accumulation of tau protein.

Beta amyloid is the main component of senile plaques which are more commonly known as Alzheimer’s plaques. It is made by an amino acid protein which is part of a larger protein called the Amyloid Precursor Protein, made by neurons and other brain cells. Defective clearance of this results in accumulation in the brain, resulting in α-β plaques. Buildup of these Amino acid plaques is toxic to neurons and can cause long term potency, damage to synapses and eventual death of neurons.

Tau protein is the main component of neurofibrillary tangles. Is it also known as over-phosphorylated microtubule associated protein tau. Neurofibrillary tangles occur when pairs of tau protein filaments twist around one another which ultimately interferes with cellular functions by displacing organelles and distorting placement of microtubules The end result is impaired axon transport which further disrupts nutrition of axons and dendrites.

Most cases of Alzheimer’s show a combination of the 2 but there are variations where one is seen more than the other.

Clinical Manifestations

Mild Alzheimer disease

· Memory loss

· Confusion about the location of familiar places

· Taking longer to accomplish normal activities of daily living

· Trouble managing handling money and paying bills

· Weakened judgment, often resulting in poor decision making

· Loss of impulsiveness and sense of drive

· Mood and personality changes

· Increased anxiety

Moderate Alzheimer disease

· Increasing memory loss and confusion

· Shortened attention span

· Problems recognizing friends and family members

· Difficulty with language

· Problems with reading, writing, working with numbers

· Difficulty organizing thoughts and thinking logically

· Inability to learn new things or to handle new or unexpected situations

· Restlessness, agitation, irritability, anxiety, tearfulness

· Wandering, especially in the late afternoon or at night

· Repetitive statements or movement; occasional muscle twitches

· Hallucinations, delusions, suspiciousness or paranoia

· Loss of impulse control: Shown through behavior such as undressing at inappropriate times or places or vulgar language

· Perceptual-motor problems: Such as trouble getting out of a chair or setting the table

Severe Alzheimer disease

· Weight loss

· Seizures, skin infections, difficulty swallowing

· Groaning, moaning, or grunting

· Increased sleeping

· In bed all or almost all the time

· Lack of bladder and bowel control

· Unable to recognize loved ones

· Unable to communicate

· Dependent on others to do all care for them

· Identity disappears

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Risk Factors

· Age

  • Risk increases greatly after age 65 and even more after age 85
  • Family history and genetics
  • If a first degree relative (parent or sibling) have AD your risk of developing it increases
  • If there is a mutation in one of the three genes associated with AD that person is basically guaranteed to inherit AD

· Sex

  • Women live longer so seem to be more likely to develop AD

· Mild cognitive impairment

· Past head trauma

  • Severe or repeated head trauma

· Lifestyle and heart health

  • Evidence suggests that the same factors that put you at risk for heart disease increase your risk for AD
  • Lack of exercise, smoking, high blood pressure, high blood cholesterol, elevated homocysteine levels, poorly controlled diabetes, diet lacking in fruits and vegetables

· Reduce risks

  • Lifelong learning and social engagement
  • Higher levels of formal education, stimulating job, mentally challenging leisure activities such as reading/playing games/playing a musical instrument, frequent social interactions


Currently, MRI is the preferred method of diagnosis because the 3D images help doctors better see the brain and its possibly affected structures such as the hippocampus. CT scans can be used to detect cerebral atrophy but that isn’t a key factor in diagnosing AD because patients may or may not have cerebral atrophy. PET scans are also used when diagnosing AD by detecting the “senile plaques” that are left behind. Doctors also try to detect the function of the blood-brain barrier because in some cases, mostly involving men, the disruption of its function is a sign of Alzheimer’s progression as well as show damage within other body systems such as the kidneys.

Doctors have been developing different methods for early detection of Alzheimer’s and they have found they may be able to test blood for neuronal protein up to ten years before symptoms appear. The protein is called “insulin receptor substrate-1 (IRS-1)” and it is important because brain insulin resistance commonly occurs in people with AD. "By measuring these proteins in the bloodstream, we were able to differentiate patients with AD from controls with almost 100% accuracy, and there is good hope that we may be able to predict the disease before clinical symptoms begin because these proteins are already abnormal when you look at them up to 10 years in advance," Dr Kapogiannis said in an interview with Medscape Medical News. It is not 100% effective yet but they are hoping that a blood test will be what it takes to diagnose AD in the future.

Alzheimer’s Is Not Normal Aging — And We Can Cure It | Samuel Cohen | TED Talks


Currently scientists have no found a cure for Alzheimer’s disease. Most patients are prescribed a drug to help maintain a clear cognitive mindset and memory. Two popular medications used for memory loss are cholinesterase inhibitors and memantine. Examples of dugs include Aricept, Exelon, Razadyne, and Namenda. The cholinesterase inhibitors wok by limiting acetylcholine breakdown and can delay symptoms for up to 12 months. Memantine works by regulating glutamate which is involved with learning and memory. However, it is common for patients to have side effects such as headache, dizziness, and confusion while taking memantine.

Alzheimer’s affects the communication between cells in the brain which causes the memory loss and cognitive instability. There have been no discoveries on how to stop this deterioration in the brain, however, these medications help to minimize the deterioration and symptoms as much as possible. They do this by targeting certain chemicals in cells that aid in cell communication.


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