May 01 2020
Nanotechnology to Treat Alzheimer’s Disease
This is a very cool study, with the massive caveat that it is extremely preliminary – but scientists have concluded an in vitro study of nanodevices that can reduce one of the pathological changes thought to be a significant cause of Alzheimer’s disease. This has to be put into context, but let me first describe what they did.
Alzheimer’s disease (AD) is a neurodegenerative disorder that affects the brain diffusely. Little by little brain cells die, the brain atrophies, and cognitive ability slowly declines causing dementia. The disease affects about 10% of people over 65, producing a huge burden on individuals, families, and society. As our population ages, it is becoming even more prevalent. There is extensive research on how Alzheimer’s disease progresses, looking for clues that might lead to an effective treatment. However, it has proven a tough nut to crack. We have many clues, but nothing that has lead to a treatment that can prevent, stall, or reverse the neurodegeneration. It is, in short, a complex disease.
One piece of this complex puzzle is the β-amyloid peptide (Aβ), which is a breakdown product of an amyloid protein precursor. The simple version is that this peptide is normally cleared from brain cells as a waste product, but in some individuals it is not sufficiently cleared and there is enough hanging around to form conglomerations or clumps of the protein. These clumps form plaques, which are a major pathological sign of AD. However, the picture is more complex than that. The amount of plaques in the brain don’t necessarily correlate with the severity of the dementia in AD, so it is clearly not the whole picture. More recent studies have found:
Substantial evidence now indicates that the solubility of Aβ, and the quantity of Aβ in different pools, may be more closely related to disease state. The composition of these pools of Aβ reflects different populations of amyloid deposits, and has definite correlates with the clinical status of the patient.
There are also pathological processes in AD that are not related to amyloid plaques, so again we are only dealing with part of the picture here. Still, researchers have been looking for ways to prevent plaque formation as a possible way to slow, stop, or even reverse AD. So far nothing has led to an approved treatment. (Current treatments for AD are only symptomatic.)