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Amyotrophic lateral sclerosis
von Hippel-Lindau disease
Acoustic neuroma (schwannoma)
Adult brain tumors
Pediatric brain tumors
Transient ischemic attack
Cavernous sinus thrombosis
Spinocerebellar ataxia (NORD)
Tethered spinal cord syndrome
Lewy body dementia
Normal pressure hydrocephalus
Acute disseminated encephalomyelitis
Central pontine myelinolysis
JC virus (Progressive multifocal leukoencephalopathy)
Idiopathic intracranial hypertension
Opsoclonus myoclonus syndrome (NORD)
Restless legs syndrome
Early infantile epileptic encephalopathy (NORD)
Cauda equina syndrome
Treponema pallidum (Syphilis)
Vitamin B12 deficiency
Concussion and traumatic brain injury
Spinal muscular atrophy
Carpal tunnel syndrome
Thoracic outlet syndrome
Lambert-Eaton myasthenic syndrome
Adult brain tumors: Pathology review
Central nervous system infections: Pathology review
Cerebral vascular disease: Pathology review
Congenital neurological disorders: Pathology review
Dementia: Pathology review
Demyelinating disorders: Pathology review
Headaches: Pathology review
Movement disorders: Pathology review
Neurocutaneous disorders: Pathology review
Neuromuscular junction disorders: Pathology review
Pediatric brain tumors: Pathology review
Seizures: Pathology review
Spinal cord disorders: Pathology review
Traumatic brain injury: Pathology review
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Jim's story: The dementia guide
5 A's of Alzheimer's Disease
Alzheimer's Disease Assessment (Early Symptoms)
Alzheimer's Disease Assessment (Late Symptoms)
Alzheimer's Disease Interventions
Alzheimer Disease & Dementia
Alzheimer disease p. 566
amalyoidosis in p. 214
Down syndome and p. 61
drug therapy for p. 239, 566
labs/findings p. 730, 736
neurotransmitters for p. 508
ventriculomegaly with p. 538
for Alzheimer disease p. 566
Alzheimer disease drugs p. 566
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.
Another big part of alzheimer disease though, are tangles, and these are actually found inside the cell, as opposed to the beta-amyloid plaques.
Just like other cells, neurons are held together by their cytoskeleton, which is partly made up of microtubules, these track-like structures that essentially act like a minecart shipping nutrients and molecules along the length of the cell.
A special protein called tau makes sure that these tracks don’t break apart, kind of like railway ties.
Although again, it’s not completely understood, it’s thought that the beta amyloid plaque build-up outside the neuron, initiates pathways inside the neuron that leads to activation of kinase, an enzyme that transfers phosphate groups to the tau protein.
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