Alzheimer’s disease (AD) brains have two characteristic findings: senile plaques and neurofibulary tangles. While the complete mechanism of AD is unknown, the plaques– aggregations of beta-amyloid proteins and glial cells — are at the very least diagnostically significant.
The plaques and the tangles eventually cause gross atrophy in particular anatomic regions:
Definitive diagnosis, though, requires an invasive biopsy. As such, histology is usually done postmortem and yields slides like this:
AD plaques. Note the globular structures in the middle and on top.
Atrophy is only obvious in late-stage AD and functional differences are suggestive at best. It’d be great if we could florescently tag proteins/genes in brains like we can everywhere else in the body. Unfortunately, brains are typically off-limits due to the blood-brain barrier (BBB).
Harvard researchers, though, decided to try anyways. They attached a MRI probe to a short DNA sequence that is complemtary to a protein expressed in glial cells (the same kind of cells that aggregate around the plaques in AD are made of) and eyedropped it into rats. They then injured the rats via puncture wound and/or stroke to bypass the BBB and induce glial cell localization. Low and behold, the MRIs effectively reported a biopsy confirmed aggregation of glial cells.
It’d be interesting for them to try it with a beta-amyloid DNA sequence attached to the probe. Their methodology could prove useful in the early detection of AD (and other diseases) provided they find a way to bypass the BBB without injuring people.