ROUGH CUTS: What we know about Alzheimer’s and other brain disorders by Robert Hickey, USA TODAY The brain is an amazing machine, but it is also one that can suffer from serious injuries, chronic illness, and even death.
As it ages, our brains are constantly exposed to new things, new stresses, and new challenges.
We may have trouble learning to think clearly, to plan ahead, to cope with stress.
And as we age, we also experience cognitive decline and damage, from mild dementia to more severe forms of dementia.
The causes and cures for some of these problems are hard to pinpoint.
But the common thread is that as we get older, we’re increasingly exposed to the world in ways we haven’t seen in years.
Our brains can be fragile, and the damage they can cause is a byproduct of our years of life.
Alzheimer’s disease is an example.
We now know that the brain is much more susceptible to damage caused by Alzheimer’s than by other disorders, including Parkinson’s disease, diabetes, and some cancers.
We also know that as you age, the brain’s repair mechanisms begin to degrade.
This is not a surprise, since these are the same mechanisms that are responsible for repair in the heart and muscles.
As we age and lose the ability to fight infections, we are also less likely to develop certain cancers, as well as chronic conditions such as cancer of the pancreas and liver.
And with Alzheimer’s, the damage that occurs to the brain becomes more serious.
The brain’s neuroplasticity, the ability of the brain to make new connections and to adapt to new situations, is weakened.
This may be why it is difficult to say whether a brain injury or a stroke will make you lose your memory or skills.
Or how much the damage to the connections of the cerebrum will hurt your speech, coordination, and motor skills.
It is also why, in some cases, people with dementia, such as Alzheimer’s patients and stroke survivors, often experience difficulties in their daily activities.
Some researchers are looking at ways to improve brain repair.
In 2005, a group of scientists led by Michael Eichler at the University of California, Los Angeles, and colleagues showed that the immune system is critical to repairing the brain, which is why a person with an infection, such the flu, has an increased risk of developing Alzheimer’s.
This suggests that, in addition to strengthening the immune response, there may be ways to modify the brain so that it is more resilient to injury.
The new research by Eichlers team has focused on a protein called MMP-1, which has been implicated in the repair of nerve cells in the brain.
This protein is activated by a chemical called tau, which occurs naturally in the blood.
Tau is part of the protein that protects nerve cells from injury.
It also helps cells keep their DNA.
Taurine, a tau receptor antagonist, was used to test whether tau could be altered in mice and whether this would improve the repair process.
They found that the mice treated with taurine were less susceptible to the effects of tau in the damaged areas of the brains of the mice with Alzheimer.
The researchers think this may be because of a mechanism called calcium signaling.
In some brain cells, calcium signals are produced to activate proteins that repair damage to neurons.
When the neurons are damaged, the cells are unable to make calcium, and they die.
In a similar way, the inflammation of the damaged area of the spinal cord, called microglia, causes inflammation of neurons, causing them to die.
Microglia cells are normally responsible for the repair that occurs when cells in other parts of the body become injured.
But when these cells become damaged, they can’t make enough calcium to repair the damage.
The inflammation can then lead to microglial activation.
When this happens, the microglium secrete calcium, which helps cells repair the damaged brain tissue.
The findings of the new research suggest that, to repair a damaged brain, there needs to be a protein that can help to repair damage and maintain the connections between the damaged tissue and surrounding cells.
In the past, it was thought that microgliosis was responsible for restoring damaged connections, such that a person who had a stroke or a heart attack could recover.
But this is not what happens when the brain receives injury.
For this reason, it has been proposed that, as we grow older, microglioid signaling is reduced and we lose the abilities to restore connections.
The team’s research, however, shows that the proteins that protect neurons from injury can still be repaired.
So they are now exploring ways to strengthen these connections.
A study by Echols and colleagues recently reported that they found a protein, TPA-1A, that was able to restore microglius and microglias in mice.
They also found that TPA1A restored the ability, in the hippocampus, to make connections