Independent Research: Alzheimer's Disease

I am currently an undergraduate student that will be working in a bioinformatics lab and I will be doing research on Alzheimer's Disease. Alzheimer's Disease is a neurodegenerative disorder in which the misbehavior of anchoring proteins within the axon of neurons cause the microtubules that span the length of the axon fall into disarray and the neuron is thus unable to function correctly (as in communicate) and will eventually die. This then manifests through changes in memory, behavior, and personality change. It is one of the forms of dementia that develops after age 65. I will be looking at this problem through genetic and neurological lenses.

I plan to use this blog to chronicle my research process which will include general summaries of what I read as well as questions I can ask.

Now to begin.

According to this overview article in NINDS, there is currently research being done on beta-amyloid plaque development and how abnormal tau proteins cause neurofibrillary tangles characteristic of AD. More research is exploring the associated precursors to AD, such as heightened cholesterol and heightened blood pressure. What are other lines of current research into AD? What genetic research is being done?

Beta-amyloid plaques are a distinguishing phenotype of AD. Amyloids are cut-up proteins that occur naturally in cells. Beta-amyloids are protein bits snipped from the amyloid precursor protein. Beta-amyloid plaques are the congregation and grouping of these beta-amyloids to form hard, insoluble structures that then damage neurons. Why and how do beta-amyloid plaques damage neurons? Why causes the formation of beta-amyloid plaques? Is there a genetic basis?

Neurofibrillary tangles result from abnormalities in a protein called tau, which is the building-block for building microtubules which are key in transporting materials through the axon of neuron. What is the genetic basis for the abnormality of tau?

Currently there are no medications that slow the progression of AD, however there are some medications that treat the disease, however their effects are transient on the scale of a few months and a few years. They aid in maintaining memory, thinking, and speaking skills. The medications for mild to moderate AD are Donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne). The medication for severe AD is memantine (Namenda). How do each of these drugs act? How were they developed?

Here is another source I may find more helpful information.

This concludes my general research on Alzheimers in general. I was directed to look into the ADNI research project as well. The following will include my research on that project.

ADNI is the Alzheimer's Disease Neuroimaging Initiative. The overview of the initiative was best said on its home site:

ADNI investigates the relationships among the clinical, cognitive, imaging, genetic and biochemical biomarker characteristics of the entire spectrum of Alzheimer’s disease (AD), as the pathology evolves from normal aging through very mild symptoms, to mild cognitive impairment (MCI), to dementia. ADNI will inform the neuroscience of AD, identify diagnostic and prognostic markers, identify outcome measures that can be used in clinical trials, and help develop the most effective clinical trial scenarios.

What are the clinical, cognitive, imaging, genetic and biochemical biomarker characteristics of Alzheimer's disease?

ADNI conducts longitudinal studies using clinical, MRI, fMRI, biomarker studies (genetic and "biochemical" what is a biochemical biomarker?).

This is where I stop until next time. I will come back to this and add to this post and possibly split it into multiple posts for the purposes of cohesion and focus.