Biology Series 1: Alzheimer’s Disease
Overview - What is
Alzheimer’s Disease (AD)?
AD is a condition in which one slowly loses ones memories, personality
and sense of self. It is named after Dr. Alois Alzheimer who
characterized this disease in 1907.
The face of AD
The cost of AD:
$61 billion annually.
The Physical Mechanism of AD
Senile: being of a certain age.
Dementia: a condition that severely impairs both and long term memory
as well as at least one other mental process (judgment, abstract
thinking, language, recognition, personality, etc.) which interfere
with daily living.
The Physical Mechanism of AD.
Plaques: sticky, gunky, circular deposits that form around
neurons (nerve cells). The major component of plaque is a
molecule called “amyloid-beta” or A-beta, one of several small
molecules that come from a large protein, called “amyloid precursor
Tangles: Physical changes that occurs inside neurons during the
course of the disease. When a tangle forms inside of a neuron, it
is always damaging and leaves the neuron twisted and deformed, and
unable to function as efficiently as before.
Suspect # 1: Plaques
The formation of “amyloid-beta” or A-beta into plaques around brain
neurons cause neuronal networks to deteriorate in AD patients.
Suspect #2: Tangles
The nearly indestructible fibers that clog up tangle bearing neurons
cause the neuron to lose integrity of its shape, thereby disrupting the
intricately connected neurons that communicate with each other to
produce meaningful mental activity.
Suspect #3: Conspirators
The combination of both plaques and tangles interacting with each other
to slowly tear apart the intricate tapestry of the brian.
The Genetics of AD.
Familial versus sporadic AD
Familial AD: If AD ran in families, it is considered as Familial
AD. (25% ~ 40%)
Sporadic AD: Patients who did not have a family member afflicted
with AD are considered to have “sporadic AD.”
The Genetics of AD.
Less than 10% of the total cases of AD is
Early-Onset AD. It is caused by inheriting mutations in three
genes encoding for Amyloid Precursor Protein (APP),
Presenilins-1 (PS-1), and Presenilins-2 (PS-2).
Brain neuronal network is damaged by the formation
of plaques due to mutations in these genes which lead to AD prior to
reaching the age of senility.
APOE and Late-Onset AD, (90% of AD)
APOE gene was found associated with a large number
of Late-Onset AD patients.
The E4 form of APOE gets stuck to the plaques more
easily than the other forms, making individuals with E4 more likely to
have damage to their neuronal
AD and Environment.
The environment is a factor that mediates a person’s
interactions with the physical world .
Weakening the immune system may help prevent AD.
Mental activity (study) strengthens
connections between neurons and may decrease the risk for developing
Current and Future Strategies for
Three drugs with FDA approval now:
Cognex, Aricept and Exelon.
Increasing the efficiency of communication between
neurons, but only work for a subset of the AD, and only for the first
few months to up to the first two years
that the patient has AD.
Preventing or removing plaques
The development of a vaccine that might make one’s immune system strong
enough to block plaque formation.
Suppress the immune system.
The use of anti-oxidants. (eliminate free radicals)
The use of growth factors. (nerve growth factor)