Cause of Alzheimer"s Disease
Alzheimer's disease is a degenerative brain disease that slowly deteriorates memory and cognitive abilities.
It is the most common cause of dementia with 10% of the population over 65 years of age and 50% of those over 85 having Alzheimer's disease.
Research has also determined that the incidence of dementia almost doubles every 5 years for those in the 90 and older range.
With the first of the baby boomers now reaching the age of 65, a large portion of the American population will be in their 10th and 11th decades of life in about 25-30 years.
This means that the disease will become a larger health concern for our population in the coming decades.
The cause of Alzheimer's disease is unknown, but the most promising framework to understanding the disease has been through the "amyloid cascade hypothesis".
This hypothesis states that the disease is genetically caused by an increased production of amyloid-beta peptides due to a missense mutation in the amaloid precursor proten (amaloid-beta peptide's precursor).
In a healthy brain, production of these otherwise normal proteins happen in such a pace that the body can easily break them down and eliminate them.
Under this increased production, however, the body is unable to deal with or adequately remove the amyloid-beta peptide.
This leads to amyloid plaque accumulation between the neurons (nerve cells) of the brain which eventually causes neuronal death.
The "amyloid cascade hypothesis" postulates that this plaque accumulation is the root cause of Alzheimer's disease.
Although the "amyloid cascade hypothesis" does much in trying to explain the cause of Alzheimer's disease, it is still incomplete.
The link between amyloid plaque accumulation and the development of neurofibrillary tangles (the primary marker for Alzheimer's disease), for example, is not fully accounted for in the hypothesis.
It has been postulated that oxidative damage due to free radicals in the brain may also play a crucial role in the development of Alzheimer's disease.
Neurons are particularly vulnerable to attacks from free radicals for a few reasons: (1) they have low natural antioxidant count, (2) their membranes contain high proportion of polyunsaturated fatty acids (a type of fat very susceptible to oxidative damage), and (3) cellular processes in the brain require a great deal of oxygen.
People with Alzheimer's have shown to have oxidation of both mitochondrial DNA as well as nuclear DNA (although to a lesser extent).
They have a greater degree of protein oxidation as compared to healthy individuals.
Also lipid peroxidation is increased in the brains of those with Alzheimer's.
Beta-amyloid and oxidation seem to not be completely mutually exclusive properties in regards to Alzheimer's disease.
It has been shown that the oxidative process has the capability to aggregate beta-amyloid.
Beta-amyloid itself is also a source of free radicals.
One hypothesis is that beta-amyloid actually acts via the production of free radicals to induce the neurodegenerative process.
It is the most common cause of dementia with 10% of the population over 65 years of age and 50% of those over 85 having Alzheimer's disease.
Research has also determined that the incidence of dementia almost doubles every 5 years for those in the 90 and older range.
With the first of the baby boomers now reaching the age of 65, a large portion of the American population will be in their 10th and 11th decades of life in about 25-30 years.
This means that the disease will become a larger health concern for our population in the coming decades.
The cause of Alzheimer's disease is unknown, but the most promising framework to understanding the disease has been through the "amyloid cascade hypothesis".
This hypothesis states that the disease is genetically caused by an increased production of amyloid-beta peptides due to a missense mutation in the amaloid precursor proten (amaloid-beta peptide's precursor).
In a healthy brain, production of these otherwise normal proteins happen in such a pace that the body can easily break them down and eliminate them.
Under this increased production, however, the body is unable to deal with or adequately remove the amyloid-beta peptide.
This leads to amyloid plaque accumulation between the neurons (nerve cells) of the brain which eventually causes neuronal death.
The "amyloid cascade hypothesis" postulates that this plaque accumulation is the root cause of Alzheimer's disease.
Although the "amyloid cascade hypothesis" does much in trying to explain the cause of Alzheimer's disease, it is still incomplete.
The link between amyloid plaque accumulation and the development of neurofibrillary tangles (the primary marker for Alzheimer's disease), for example, is not fully accounted for in the hypothesis.
It has been postulated that oxidative damage due to free radicals in the brain may also play a crucial role in the development of Alzheimer's disease.
Neurons are particularly vulnerable to attacks from free radicals for a few reasons: (1) they have low natural antioxidant count, (2) their membranes contain high proportion of polyunsaturated fatty acids (a type of fat very susceptible to oxidative damage), and (3) cellular processes in the brain require a great deal of oxygen.
People with Alzheimer's have shown to have oxidation of both mitochondrial DNA as well as nuclear DNA (although to a lesser extent).
They have a greater degree of protein oxidation as compared to healthy individuals.
Also lipid peroxidation is increased in the brains of those with Alzheimer's.
Beta-amyloid and oxidation seem to not be completely mutually exclusive properties in regards to Alzheimer's disease.
It has been shown that the oxidative process has the capability to aggregate beta-amyloid.
Beta-amyloid itself is also a source of free radicals.
One hypothesis is that beta-amyloid actually acts via the production of free radicals to induce the neurodegenerative process.
