Hope that it could be so simple...

Tests on brain samples from dead people have strengthened claims that Alzheimer's disease may be caused by the same virus that causes cold sores.
"We think the virus is a very strong risk factor for the disease," says Ruth Itzhaki of the University of Manchester, UK – head of the team leading the investigation.

If confirmed by further research, the finding opens up the possibility of treating Alzheimer's with acyclovir, a cheap antiviral drug used to treat cold sores, or even vaccinating against it.
One of the hallmarks of the incurable disease is the presence of sticky plaques, which seem to clog up the working of the brain and result in dementia.
Brain maps
The virus that causes cold sores – Herpes simplex type 1 – was found in 90% of plaque samples from six patients who had died of Alzheimer's disease.
The virus was also found in 80% of the plaques in brain tissue from five "control" patients who didn't die of Alzheimer's, although they had far fewer plaques overall than the patients.
However, the most convincing evidence that the virus is linked with the disease came from scans mapping the whereabouts of the virus across the whole brain. These showed that, in the Alzheimer's patients, 72% of the virus found was in the plaques, compared with just 24% in the non-Alzheimer's brains.
"It's very specifically located in the plaques, so it strongly supports the likelihood that the virus is a major cause of plaque formation," says Itzhaki.
In earlier studies, Itzhaki's team demonstrated that when healthy brain cells are grown in culture and infected with HSV-1, they accumulate the same amyloid beta protein that is found in plaque.
Itzhaki's team followed that up by showing that amyloid beta plaques formed in the brains of mice deliberately infected with the virus.
Now the new results provide direct evidence that the same happens in the brains of people with Alzheimer's.
Antiviral attack
Itzhaki found that all six patients had inherited at least one copy of APOE-ε4 – a gene variant previously linked with higher risk of Alzheimer's.
She speculates that the variant somehow impairs clearance of the amyloid protein from brain cells infected by the virus, or perhaps leads to excessive production of the protein in those cells. "It either enhances the damage, or makes the cells less efficient at repairing it," she says.
"We suggest the virus enters the brain in the elderly as their immune systems decline, and establishes a latent infection from which it is repeatedly reactivated by events such as stress, immunosuppression and brain inflammation," says Itzhaki.
In normal brains, the infection is kept under control, but in patients with the APOE-ε4 gene variant, the virus gets the upper hand, leading to Alzheimer's.
Already, Itzhaki has followed up her findings to see if antiviral drugs like acyclovir reduce symptoms. "We've used the antivirals in infected human cells and found it reduced the burden of beta amyloid," she says. "It was obvious by eye that there were great reductions."
The next step, says Itzhaki, is to raise funds for a clinical trial. "All the evidence we have suggests it would work," she says.
Not everyone is convinced, however.
"Although the new research provides some additional evidence supporting a link between the herpes virus and Alzheimer's disease, there is considerable uncertainty around whether this is a promising avenue of research," says Clive Ballard, director of research at the UK Alzheimer's Society.
Journal reference: Journal of Pathology (DOI: 10.1002/path.2449)