Alzheimer’s Disease

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1
is a neurodegenerative disease that causes memory loss, behavioral changes and immobility
Alzheimer’s Disease
2
Nearly 5% of the adult population aged () will have Alzheimer’s disease
65 years
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is not a normal part of the aging process.
Dementia
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PET scan –
Positron Emission Tomography
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Yellow color signifies
Acetylcholine
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The following are believed to speed the progression of
Alzheimer’s disease:
○ Cerebrovascular disease
○ High blood pressure
○ Diabetes
○ Sleep apnea
○ Parkinson disease
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– plays a major role in the progression of AZD
Diabetes Mellitus
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Alzheimers disease is also called
type 3 diabetis mellitus
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– stop breathing while you're sleeping → disrupt
O2 level particularly in brain → loss of neurons
Sleep apnea
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• HTN: AZD + HTN → faster onset of AZD
Cerebrovascular Disease
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- low Dopamine inc Ach → depigmentation
of substantia nigra (associated w/ AZD)
Parkinson's disease
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Alzheimer’s disease damages the
hippocampus
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Familial Alzheimer’s disease is associated with the gene that
makes the protein
apolipoprotein E (ApoE)
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The disease causes cholinergic nerve cells in the brain to
die
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() shrinks in size and the ability to think and function diminishes.
cerebral cortex
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Abnormal structures, called (?) , develop in the brain
plaques and tangles
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- resp for memory and learning
− If it shrinks → diminished ability to think and function
Hippocampus
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- characteristic ridges (narrows in AZD)
Gyri
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- spaces between gyri (widens in AZD)
Sulci
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: are sticky, dense substances composed of protein
Plaques
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Plaques: are sticky, dense substances composed of protein called
beta amyloid
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- fill the spaces between neurons in the
brain and interfere with the transmission of signals between the neurons.
Plaques
beta amyloid
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: are twisted fibers and are made of protein clumps
called tau
Tangles
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Tangles: are twisted fibers and are made of protein clumps
called
tau
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Formation of Plaques:
In the cell membrane of neurons, there is the
Amyloid precursor proteins
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one side located outside the other is inside the cell membrane
Amyloid precursor proteins (APP)
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• Regulates growth of neurons
• Repairing neurons after injury
Amyloid precursor proteins (APP)
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After serving its purpose → breakdown by 2 enzymes
gamma secretase and αlpha secretase
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→ insoluble fragments → clumping of fragments outside neurons →
forming β-amyloid plaques (blocked in between neurons
→ disrupting signaling)
Problem if gamma secretase pairs w/ β secretase
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– clumping in the soma (inside neurons – specifically in cell body
Tangles
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– normal in the body
Tau proteins
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stabilize neurons (hold cell membrane together)
• Problem: instead of stabilizing neurons, Tau kills neurons in AZD
Tau proteins
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– clumping of Tau proteins → blocking of neurons → disrupting signaling
Neurofibrillary tangles
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