WORK ON BUILDING NEW NEURONS
Friday, March 4, 2011
One strand of stem cell research is learning how to construct exactly
the type of cell needed: "researchers for the first time have
transformed a human embryonic stem cell into a critical type of neuron
that dies early in Alzheimer's disease and is a major cause of memory
loss. This new ability to reprogram stem cells and grow a limitless
supply of the human neurons will enable a rapid wave of drug testing
for Alzheimer's disease, allow researchers to study why the neurons
die and could potentially lead to transplanting the new neurons into
people with Alzheimer's. ... These critical neurons, called basal
forebrain cholinergic neurons, help the hippocampus retrieve memories
in the brain. In early Alzheimer's, the ability to retrieve memories
is lost, not the memories themselves. There is a relatively small
population of these neurons in the brain, and their loss has a swift
and devastating effect on the ability to remember. ... Now that we
have learned how to make these cells, we can study them in a tissue
culture dish and figure out what we can do to prevent them from dying.
... This technique to produce the neurons allows for an almost
infinite number of these cells to be grown in labs, allowing other
scientists the ability to study why this one population of cells
selectively dies in Alzheimer's disease. ... The ability to make the
cells also means researchers can quickly test thousands of different
drugs to see which ones may keep the cells alive when they are in a
challenging environment. ... [Researchers] demonstrated the newly
produced neurons work just like the originals. They transplanted the
new neurons into the hippocampus of mice and showed the neurons
functioned normally. The neurons produced axons, or connecting fibers,
to the hippocampus and pumped out acetylcholine, a chemical needed by
the hippocampus to retrieve memories from other parts of the brain."
ALZHEIMER'S PLAQUE AND THE LIVER
Friday, March 4, 2011
Interesting research reported via ScienceDaily: "Unexpected results
from a [recent study] could completely alter scientists' ideas about
Alzheimer's disease - pointing to the liver instead of the brain as
the source of the 'amyloid' that deposits as brain plaques associated
with this devastating condition. The findings could offer a relatively
simple approach for Alzheimer's prevention and treatment. ... The
product of [the mouse gene corresponding to a gene known to predispose
humans carrying particular variations of it to develop early-onset
Alzheimer's disease], called Presenilin2, is [involved] in the
generation of pathogenic beta amyloid. Unexpectedly, heritable
expression of Presenilin2 was found in the liver but not in the brain.
Higher expression of Presenilin2 in the liver correlated with greater
accumulation of beta amyloid in the brain and development of
Alzheimer's-like pathology. ... This finding suggested that
significant concentrations of beta amyloid might originate in the
liver, circulate in the blood, and enter the brain. If true, blocking
production of beta amyloid in the liver should protect the brain. ...
mice were administered imatinib [which] has poor penetration of the
blood-brain barrier in both mice and humans. ... Because it doesn't
penetrate the blood-brain barrier, we were able to focus on the
production of amyloid outside of the brain and how that production
might contribute to amyloid that accumulates in the brain, where it is
associated with disease. ... the drug dramatically reduced beta
amyloid not only in the blood, but also in the brain where the drug
cannot penetrate. Thus, an appreciable portion of brain amyloid must
originate outside of the brain, and imatinib represents a candidate
for preventing and treating Alzheimer's."
Friday, March 4, 2011
One strand of stem cell research is learning how to construct exactly
the type of cell needed: "researchers for the first time have
transformed a human embryonic stem cell into a critical type of neuron
that dies early in Alzheimer's disease and is a major cause of memory
loss. This new ability to reprogram stem cells and grow a limitless
supply of the human neurons will enable a rapid wave of drug testing
for Alzheimer's disease, allow researchers to study why the neurons
die and could potentially lead to transplanting the new neurons into
people with Alzheimer's. ... These critical neurons, called basal
forebrain cholinergic neurons, help the hippocampus retrieve memories
in the brain. In early Alzheimer's, the ability to retrieve memories
is lost, not the memories themselves. There is a relatively small
population of these neurons in the brain, and their loss has a swift
and devastating effect on the ability to remember. ... Now that we
have learned how to make these cells, we can study them in a tissue
culture dish and figure out what we can do to prevent them from dying.
... This technique to produce the neurons allows for an almost
infinite number of these cells to be grown in labs, allowing other
scientists the ability to study why this one population of cells
selectively dies in Alzheimer's disease. ... The ability to make the
cells also means researchers can quickly test thousands of different
drugs to see which ones may keep the cells alive when they are in a
challenging environment. ... [Researchers] demonstrated the newly
produced neurons work just like the originals. They transplanted the
new neurons into the hippocampus of mice and showed the neurons
functioned normally. The neurons produced axons, or connecting fibers,
to the hippocampus and pumped out acetylcholine, a chemical needed by
the hippocampus to retrieve memories from other parts of the brain."
ALZHEIMER'S PLAQUE AND THE LIVER
Friday, March 4, 2011
Interesting research reported via ScienceDaily: "Unexpected results
from a [recent study] could completely alter scientists' ideas about
Alzheimer's disease - pointing to the liver instead of the brain as
the source of the 'amyloid' that deposits as brain plaques associated
with this devastating condition. The findings could offer a relatively
simple approach for Alzheimer's prevention and treatment. ... The
product of [the mouse gene corresponding to a gene known to predispose
humans carrying particular variations of it to develop early-onset
Alzheimer's disease], called Presenilin2, is [involved] in the
generation of pathogenic beta amyloid. Unexpectedly, heritable
expression of Presenilin2 was found in the liver but not in the brain.
Higher expression of Presenilin2 in the liver correlated with greater
accumulation of beta amyloid in the brain and development of
Alzheimer's-like pathology. ... This finding suggested that
significant concentrations of beta amyloid might originate in the
liver, circulate in the blood, and enter the brain. If true, blocking
production of beta amyloid in the liver should protect the brain. ...
mice were administered imatinib [which] has poor penetration of the
blood-brain barrier in both mice and humans. ... Because it doesn't
penetrate the blood-brain barrier, we were able to focus on the
production of amyloid outside of the brain and how that production
might contribute to amyloid that accumulates in the brain, where it is
associated with disease. ... the drug dramatically reduced beta
amyloid not only in the blood, but also in the brain where the drug
cannot penetrate. Thus, an appreciable portion of brain amyloid must
originate outside of the brain, and imatinib represents a candidate
for preventing and treating Alzheimer's."