Angela
Elite member
- Messages
- 21,823
- Reaction score
- 12,329
- Points
- 113
- Ethnic group
- Italian
It's an intriguing question, but even if it is, given that it seems to run in families, there must be a predisposition to it.
See:
https://blogs.scientificamerican.co...rce=twitter&utm_campaign=SciAm_&sf209341175=1
"it is also one of the few major diseases that cannot be treated, prevented or cured. 99.6 percent of Alzheimer’s drugs developed between 2002 and 2012 failed in clinical trials, and since then, multiple treatments that appeared to be promising delivered disappointing results in trials. Despite the thousands of scientists who are conducting research on Alzheimer’s, the Food and Drug Administration hasn’t approved a new Alzheimer’s drug since 2003.Existing medications have mostly sought to inhibit the protein amyloid beta. For the past few decades, the majority of researchers have agreed that abnormal production of amyloid beta triggers the neurodegeneration that occurs in Alzheimer’s. However, the repeated failure of the drugs would appear to suggest that the so-called “amyloid beta hypothesis” may not be entirely correct. Staunch believers in the hypothesis assert that the drugs either were flawed or were not administered to patients at the right time; aggregates of amyloid beta known as plaques can form in the brain decades before people begin to exhibit symptoms of Alzheimer’s."
"Furthermore, this view is not merely speculative. According to recent hypotheses that have firm empirical support, amyloid beta may, in fact, be a tool that the brain uses in order to fight the underlying cause of Alzheimer’s: infections by pathogens, such as viruses, bacteria and fungi. Many different pathogens have been linked to Alzheimer’s; one that has been studied quite extensively is herpes simplex virus type 1 (HSV-1). In part because it is orally transmitted, this virus is very ubiquitous, present in over 67 percent of people around the world who are under age 50. The immediate effects of HSV-1 are mostly harmless: the majority of those who are infected display cold sores, and some never even exhibit any symptoms.
But in 1997, a team of scientists led by Ruth Itzhaki at the University of Manchester found that HSV-1 infection in people who have the APOE ε4gene, which is, on its own, associated with Alzheimer’s, have a much higher risk of developing the condition. More recently, Itzhaki and her colleagues have shown that HSV-1 causes a dramatic increase in amyloid beta production in infected cell cultures and furthermore that 90 percent of amyloid beta plaques contain the viral DNA of HSV-1. A large share of the research that has been conducted thus far has established a correlation between HSV-1 and Alzheimer’s but not a causal relationship. "
"In 2011, Itzhaki and her colleagues showed that the anti-herpes drug acyclovir reduces levels of amyloid beta in cell cultures that were infected with HSV-1. Last year, a study involving over 34,000 Taiwanese patients found that people who were infected with HSV-1 were 2.56 times more likely to get dementia, but that undergoing treatment for HSV-1 lowered their risk of Alzheimer’s by over 80 percent."
See:
https://blogs.scientificamerican.co...rce=twitter&utm_campaign=SciAm_&sf209341175=1
"it is also one of the few major diseases that cannot be treated, prevented or cured. 99.6 percent of Alzheimer’s drugs developed between 2002 and 2012 failed in clinical trials, and since then, multiple treatments that appeared to be promising delivered disappointing results in trials. Despite the thousands of scientists who are conducting research on Alzheimer’s, the Food and Drug Administration hasn’t approved a new Alzheimer’s drug since 2003.Existing medications have mostly sought to inhibit the protein amyloid beta. For the past few decades, the majority of researchers have agreed that abnormal production of amyloid beta triggers the neurodegeneration that occurs in Alzheimer’s. However, the repeated failure of the drugs would appear to suggest that the so-called “amyloid beta hypothesis” may not be entirely correct. Staunch believers in the hypothesis assert that the drugs either were flawed or were not administered to patients at the right time; aggregates of amyloid beta known as plaques can form in the brain decades before people begin to exhibit symptoms of Alzheimer’s."
"Furthermore, this view is not merely speculative. According to recent hypotheses that have firm empirical support, amyloid beta may, in fact, be a tool that the brain uses in order to fight the underlying cause of Alzheimer’s: infections by pathogens, such as viruses, bacteria and fungi. Many different pathogens have been linked to Alzheimer’s; one that has been studied quite extensively is herpes simplex virus type 1 (HSV-1). In part because it is orally transmitted, this virus is very ubiquitous, present in over 67 percent of people around the world who are under age 50. The immediate effects of HSV-1 are mostly harmless: the majority of those who are infected display cold sores, and some never even exhibit any symptoms.
But in 1997, a team of scientists led by Ruth Itzhaki at the University of Manchester found that HSV-1 infection in people who have the APOE ε4gene, which is, on its own, associated with Alzheimer’s, have a much higher risk of developing the condition. More recently, Itzhaki and her colleagues have shown that HSV-1 causes a dramatic increase in amyloid beta production in infected cell cultures and furthermore that 90 percent of amyloid beta plaques contain the viral DNA of HSV-1. A large share of the research that has been conducted thus far has established a correlation between HSV-1 and Alzheimer’s but not a causal relationship. "
"In 2011, Itzhaki and her colleagues showed that the anti-herpes drug acyclovir reduces levels of amyloid beta in cell cultures that were infected with HSV-1. Last year, a study involving over 34,000 Taiwanese patients found that people who were infected with HSV-1 were 2.56 times more likely to get dementia, but that undergoing treatment for HSV-1 lowered their risk of Alzheimer’s by over 80 percent."
