Alzheimer disease

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Alzheimer disease

Nervous system

Autonomic nervous system disorders

Horner syndrome

Orthostatic hypotension


Alzheimer disease


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USMLE® Step 1 questions

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High Yield Notes

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Alzheimer disease

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USMLE® Step 1 style questions USMLE

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A pathologist is examining brain biopsies from a patient who died from a neurodegenerative condition following an episode of aspiration pneumonia. A tissue sample from the patient is demonstrated below:

Image reproduced from Wikimedia Commons

Further staining reveals patchy red plaques that become yellow when viewed under polarized light. Which of the following clinical courses was most likely seen in this patient? 

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Acetylcholinesterase (AChE) inhibitors

Alzheimer disease p. 569

Alzheimer disease p. 538

amalyoidosis in p. 216

Down syndome and p. 61

drug therapy for p. 241, 569

labs/findings p. 722, 731

neurotransmitters for p. 512

ventriculomegaly with p. 540

Early-onset Alzheimer disease p. 61

Galantamine p. 241

for Alzheimer disease p. 569


Alzheimer disease drugs p. 569

Rivastigmine p. 241

Alzheimer disease p. 569


Content Reviewers

Dementia isn’t technically a disease, but more of a way to describe a set of symptoms like poor memory and difficulty learning new information, which can make it really hard to function independently.

Usually dementia’s caused by some sort of damage to the cells in the brain, which can be caused by a variety of diseases. Alzheimer’s disease, now referred to as Alzheimer disease, is the most common cause of dementia.

Alzheimer disease is considered a neurodegenerative disease, meaning it causes the degeneration, or loss, of neurons in the brain, particularly in the cortex. This, as you might expect, leads to the symptoms characteristic of dementia.

Although the cause of Alzheimer disease isn’t completely understood, two major players that are often cited in its progression are plaques and tangles.

Alright, so here we’ve got the cell membrane of a neuron in the brain. In the membrane, you’ve got this molecule called amyloid precursor protein, or APP, one end of this guy’s in the cell, and the other end’s outside the cell. It’s thought that this guy helps the neuron grow and repair itself after an injury.

Since APP’s a protein, just like other proteins, it gets used and over time it gets broken down and recycled.

Normally, it gets chopped up by an enzyme called alpha secretase and it’s buddy, gamma secretase.

This chopped up peptide is soluble and goes away, and everything’s all good.

If another enzyme, beta secretase, teams up with gamma secretase instead, then we’ve got a problem, and this leftover fragment isn’t soluble, and creates a monomer called amyloid beta.

These monomers tend to be chemically “sticky”, and bond together just outside the neurons, and form what are called beta-amyloid plaques—these clumps of lots of these monomers.

These plaques can potentially get between the neurons, which can get in the way of neuron-to-neuron signaling.

If the brain cells can’t signal and relay information, then brain functions like memory can be seriously impaired.

It’s also thought that these plaques can start up an immune response and cause inflammation which might damage surrounding neurons.

Amyloid plaque can also deposit around blood vessels in the brain, called amyloid angiopathy, which weakens the walls of the blood vessels and increases the risk of hemorrhage, or rupture and blood loss.

Here’s an image of amyloid plaque on histology, these clumps are buildups of beta amyloid, and this is happening outside the cell.


  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "Alzheimer's disease" BMJ (2009)
  5. "Early-onset Alzheimer's Disease: Nonamnestic Subtypes and Type 2 AD" Archives of Medical Research (2012)
  6. "Pathogenic tau-induced piRNA depletion promotes neuronal death through transposable element dysregulation in neurodegenerative tauopathies" Nature Neuroscience (2018)

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