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Nervous system
Amyotrophic lateral sclerosis
Neurofibromatosis
Sturge-Weber syndrome
Tuberous sclerosis
von Hippel-Lindau disease
Brain herniation
Broca aphasia
Kluver-Bucy syndrome
Wernicke aphasia
Wernicke-Korsakoff syndrome
Acoustic neuroma (schwannoma)
Adult brain tumors
Pediatric brain tumors
Pituitary adenoma
Ischemic stroke
Transient ischemic attack
Brain abscess
Cavernous sinus thrombosis
Creutzfeldt-Jakob disease
Encephalitis
Epidural abscess
Meningitis
Neonatal meningitis
Aqueductal stenosis
Cerebral palsy
Chiari malformation
Dandy-Walker malformation
Septo-optic dysplasia
Spina bifida
Spinocerebellar ataxia (NORD)
Syringomyelia
Tethered spinal cord syndrome
Alzheimer disease
Creutzfeldt-Jakob disease
Delirium
Frontotemporal dementia
Lewy body dementia
Normal pressure hydrocephalus
Vascular dementia
Acute disseminated encephalomyelitis
Central pontine myelinolysis
JC virus (Progressive multifocal leukoencephalopathy)
Multiple sclerosis
Transverse myelitis
Cavernous sinus thrombosis
Cluster headache
Idiopathic intracranial hypertension
Migraine
Tension headache
Trigeminal neuralgia
Arteriovenous malformation
Epidural hematoma
Intracerebral hemorrhage
Saccular aneurysm
Subarachnoid hemorrhage
Subdural hematoma
Essential tremor
Huntington disease
Opsoclonus myoclonus syndrome (NORD)
Parkinson disease
Restless legs syndrome
Torticollis
Early infantile epileptic encephalopathy (NORD)
Epilepsy
Febrile seizure
Brown-Sequard Syndrome
Cauda equina syndrome
Friedreich ataxia
Neurogenic bladder
Syringomyelia
Treponema pallidum (Syphilis)
Vitamin B12 deficiency
Concussion and traumatic brain injury
Poliovirus
Spinal muscular atrophy
Charcot-Marie-Tooth disease
Guillain-Barre syndrome
Bell palsy
Trigeminal neuralgia
Carpal tunnel syndrome
Erb-Duchenne palsy
Klumpke paralysis
Sciatica
Thoracic outlet syndrome
Ulnar claw
Winged scapula
Lambert-Eaton myasthenic syndrome
Myasthenia gravis
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
Alzheimer disease
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Alzheimer disease p. 569
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
for Alzheimer disease p. 569
Alzheimer disease drugs p. 569
Alzheimer disease p. 569
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.
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