FAQ about Alzheimer's disease

Q1. What is Alzheimer’s disease?
Alzheimer’s disease is the common illness that causes dementia. Dementia occurs as a set of related symptoms when the brain is damaged by disease.
The main symptom of dementia is memory loss.
Q2. Why does Alzheimer's disease occur?
In the brain of Alzheimer’s disease, protein called amyloid (β) accumulates, and the structure called senile plaques appears in the brain. Amyloid is a kind of garbage generated by brain activity.
In the initial state when amyloid begins to accumulate, the patient has not yet developed dementia. (Preclinical Alzheimer's disease)
Q3. Why does memory loss occur by Alzheimer’s disease?
The brain maintains memory by storing the memory in a place called synapse. Protein called drebrin is the necessary skeleton to maintain the memory in the synapse.
However drebrin decreases with aging even in healthy people, the decrease in drebrin is enhanced by the accumulation of amyloid. Patients with Alzheimer's disease run out of drebrin, so that memory loss occurs by blurring the function of synapses.
Q4. Why does dementia develop as Alzheimer's disease progresses?
When synapses work poorly by the decrease in drebrin because of the accumulation of amyloid, neurodegeneration occurs. After that, nerve cells die by neurofibrillary tangle that mean accumulation of tau proteins. As a result, dementia develops.
Dead nerve cells do not regenerate, so the medical condition becomes irreversible.
But the disappearance of drebrin is believed to be reversible, we expect preventing the progression of nerve cell death by the increase of drebrin.
Q5. What are the medicines for Alzheimer's disease?
Unfortunately, we have no medicine that prevent the onset of Alzheimer's disease, and that prevent the progression of dementia, except for symptomatic medicine that temporarily cure the symptoms of dementia.
Alzheimer's disease is caused by the accumulation of amyloid in the brain. Many pharmaceutical companies have tried to develop medicines (specific monoclonal antibodies and drugs that block the enzymes that make amyloid, for example) not to accumulate of amyloid in the brain for the patients of preclinical Alzheimer's disease. But it has not been successful yet.
We aim to develop treatments that prevent the progression of dementia by the medicine which prevent the disappearance of drebrin by amyloid.
In animal experiments, it is shown by diet remedies and gene expression regulation that increased drebrin improves memory loss. The new treatment for Alzheimer's disease that we are aiming for is considered to be a very promising method.