Holtzman says.

He thinks Alzheimer’s disease is a kind of garbage collection problem. As nerve

cells, or neurons, take care of business, they tend to leave their trash lying around.
They throw away A-beta, which is a leftover remnant of a larger protein that is
thought to form connections between neurons in the developing brain, but whose
role in adults is still being studied. The body usually clears away A-beta.

But sometimes, especially when cheated on sleep, the brain doesn’t get the chance to mop
up all the A-beta that the neurons produce, according to a developing consensus. A-beta
starts to collect in the small seams between cells of the brain, like litter in the gutter. If A-beta
piles up too much, it can accumulate into plaques that are thought to eventually lead to other
problems such as inflammation and the buildup of tau, which appears to destroy neurons
and lead to Alzheimer’s disease.

Neurofibrillary tangles occur when proteins become misshapen inside the neurons and potentially undermine the
delicate cellular support systems.’

There’s also the questionable use of the term “cure” in the many reports
around this. Even if the drug works 100% effectively as hoped, the damage to
the brain inflicted by Alzheimer’s and similar diseases is widespread and
severe. And the human brain, particularly if it’s quite old already, has limited
scope for repair in such circumstances. The human brain works thanks to
complex and specific networks and connections between the various areas,
and these are the result of a lifetime of development and experience.

Alzheimer’s causes widespread damage and destruction to neurons, and while

stopping the process causing it will prevent things from getting worse, it won’t
automatically mean things will get better. Even if we could somehow replace
the lost brain cells in the damaged regions (which we can’t), to claim a full
“cure”, we’d need to somehow shape and connect them so they’re exactly as
they were.

But while some drugs have reduced the accumulation of amyloid, none have yet
succeeded in stopping or reversing dementia. And amyloid doesn’t explain
everything about Alzheimer’s — not everyone with amyloid plaques has the disease.

“It’s not that amyloid is not an important factor,” said Dr. John Morris, director of
the Knight Alzheimer’s Disease Research Center at the Washington University School
of Medicine in St. Louis. “On the other hand, we’ve had some 200-plus trials since
2001 that have been negative.”

Not all trials have targeted amyloid. Some have focused on tau, a protein that, in
Alzheimer’s, forms threads that stick together in tangles inside neurons, sandbagging
their communications with one another.

Tau tangles seem to spread after amyloid accumulates into plaques between neurons.
But so far, anti-tau drugs haven’t successfully attacked Alzheimer’s itself.

Amyloid beta plaques

The brain creates Abeta with enzymes that chop a larger protein, called the amyloid precursor
protein (APP), into smaller bits. Sometimes, for reasons scientists don’t quite understand, two
APP proteins join together in a process called dimerization, which ultimately leads to increased
Abeta.
Can breaking down brain plaques prevent Alzheimer's?
Amyloid plaques are one of the defining pathologies of Alzheimer’s disease. They are
formed by the gradual build-up of a toxic protein called amyloid-beta in brain and are
observed later in the disease progression. Therefore, if amyloid plaques are detected in the
brain of an individual presenting with dementia then they likely already have Alzheimer’s
disease and breaking up the plaques will not prevent them from getting it. Studies in animals
have shown that effectively breaking up the amyloid plaques and removing the toxic
amyloid-beta from the brain will, however, reduce the disease progression and improve
memory (A study from our group demonstrated this using non-invasive scanning ultrasound:
Leinenga, G. and Götz, J., Science Translational Medicine , 2015). Unfortunately, the
restoration of memory has not been replicated in human clinical trials yet, despite the
successful clearance of amyloid-plaques. However, this may be due to other factors, such as
the design of the trials, rather than the treatments themselves. In summary, breaking up
amyloid plaques will not prevent Alzheimer’s disease but may slow down its progression.