Exploring 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 protein” (APP).  

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.
Early-Onset 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 AD.

Current and Future Strategies for Treating AD.
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.
Protecting Neurons:
Suppress the immune system.
The use of anti-oxidants. (eliminate free radicals)
The use of growth factors. (nerve growth factor)