Theory
A) General Injury
- All brains undergo neuroplasticity in response to damage. Neurons are one of the few cells in the body that do not replicate. When they are exposed to damaging ions (e.g. free radicals) following smoking a cigarette they repair themselves (use an intracellular repair protein called ‘tau’) and can branch to contact neighboring neurons. However, at some point in life this neuroplasticity will be overcome and these neurons that have branched together coalesce into a ‘neurofibrillary tangle’.
B) Alzheimer Brain
- Alzheimer disease is given to those individuals who have an inability to tolerate the neuronal damage of the cholinergic neurons within the brain. This thought to be due to faulty repair mechanisms (e.g. familial defects, no HRT in post-menopausal women, Down’s Syndrome, etc).
1. There is a high density of cholinergic neurons in the low limbic region of the brain. This is the location of the initial neuronal loss for Alzheimer’s disease. This is the beginning of loss of smell and personality change.
a) entororhinal cortex
b) amygdala
2. With time, the damage progresses to the high limbic region. This marks the beginning of amnestic Mild Cognitive Impairment.
a) association cortex of occipital-parietal lobe
b) hippocampus
3. Finally, it will spread to the high neocortex. This is the beginning of Severe Dementia.
a) frontal, parietal, anterior temporal neocortex
- At any point in time, if a person were to die from natural causes and undergo an autopsy, there would be a high concentration of neurofibrillary tangles found in the respective regions of the brain the correlate with the stage of their Alzheimer’s Disease. Likewise, certain neuroimaging studies can also be used to confirm the diagnosis; specifically the SPECT study.
C) Amyloid Neuritic Plaques
- Finally, in areas of the neuronal injury (of any sort) peptide structures called amyloid plaques can develop. An amyloid plaque is made from protein and is found outside of any neurons. In the normal population, these are found in increasing amounts as we age. What has been observed is that in the brain of a patient with Alzheimer’s disease, these amyloid plaques surround the neuronal axons that are filled with the tau repair proteins. There is a new neuroimaging test recently available called an Amyvid study which allows physicians to scan for higher than normal amount of amyloid plaques within the brain. If present, in the right clinical scenario, it could support the diagnosis of Alzheimer’s disease.