A number of approaches to Alzheimer's disease don't seek to address the underlying causes of pathology, but rather shore up crucial mechanisms that are harmed. This approach is actually very common throughout modern medicine, and it is something that I think has to change in order to improve the effectiveness of medical research and development. This is an example of the type:
"Several years ago we discovered that NAP, a snippet of a protein essential for brain formation, which later showed efficacy in Phase 2 clinical trials in mild cognitive impairment patients, a precursor to Alzheimer's. Now, we're investigating whether there are other novel NAP-like sequences in other proteins. This is the question that led us to our discovery. NAP operates through the stabilization of microtubules - tubes within the cell which maintain cellular shape. They serve as 'train tracks' for movement of biological material. This is very important to nerve cells, because they have long processes and would otherwise collapse. In Alzheimer's disease, these microtubules break down. The newly discovered protein fragments, just like NAP before them, work to protect microtubules, thereby protecting the cell."
[The researchers] looked at the subunit of the microtubule - the tubulin - and the protein TAU (tubulin-associated unit), important for assembly and maintenance of the microtubule. Abnormal TAU proteins form the tangles that contribute to Alzheimer's; increased tangle accumulation is indicative of cognitive deterioration. [Researchers tested] both the tubulin and the TAU proteins for NAP-like sequences. After confirming NAP-like sequences in both tubulin subunits and in TAU, [they then] tested the fragments in tissue cultures for nerve-cell protecting properties against amyloid peptides, the cause of plaque build up in Alzheimer patients' brains.
"From the tissue culture, we moved to a 10-month-old transgenic mouse model with frontotemporal dementia-like characteristics, which exhibits TAU pathology and cognitive decline. We tested one compound - a tubulin fragment - and saw that it protected against cognitive deficits. When we looked at the 'dementia'-afflicted brain, there was a reduction in the NAP parent protein, but upon treatment with the tubulin fragment, the protein was restored to normal levels."