Most Recent Questions and Answers courtesy of AHAF
Is it true that the stress hormone cortisol is linked with Alzheimer’s disease? Do people with anxiety disorders have an increased risk of developing Alzheimer’s?
While it is true that studies have found higher levels of the stress hormone cortisol associated with patients having dementia (such as Alzheimer’s disease) than in aged-matched control subjects, there is no hard evidence to suggest that cortisol actually causes Alzheimer’s disease pathology. Additionally, there do not appear to be any studies indicating that people with anxiety disorders are at higher risk of developing Alzheimer’s disease. Conversely, however, there appears to be a higher likelihood of developing a generalized anxiety disorder or depression following a diagnosis of Alzheimer’s disease.
Since Alzheimer’s disease is a slow progressive disease, is it possible that it is transmitted through blood transfusion from someone who is not aware that they have the disease? I have been told this could be very easily proven by checking statistical studies concerning the incidence of Alzheimer’s disease in Jehovah’s Witnesses (who do not accept blood transfusions) versus the general public.
There was actually a study performed in 1997 that examined whether a history of blood transfusions was a determining risk factor for the development of Alzheimer’s disease (AD). The investigators found no correlation between receiving blood transfusions and the development of AD (O’Meara ES et al. Neuroepidemiology, 1997; 16(2):86-93). Additionally, there is no clinical or scientific evidence to suggest that Alzheimer’s disease is transmitted through blood transfusions.
How are scientists progressing towards finding the cure for Alzheimer’s disease? What are some of the most recent experimental treatments that have been tested on patients with Alzheimer’s disease?
While a cure for Alzheimer’s disease (AD) remains elusive, there is some intriguing new research that looks hopeful. The most promising therapeutic strategies entail slowing or inhibiting the abnormally aggregated proteins—amyloid-beta and tau—from forming and/or depositing in the brain, or else removing the deposits that have already formed. For example, several drugs being tested in the laboratory are directed to a “preventative approach,” wherein the drugs work by blocking the metabolic pathway leading abnormally folded or excessive amyloid-beta or tau production. Another therapy involves a “passive immunization” approach and uses antibodies directed against beta-amyloid. (Antibodies are molecules produced by the immune system in response to foreign particles or pathogens.) The administered antibodies attach to amyloid plaques and recruit the brain’s own immune cells to aid in attacking and destroying the plaques.
Another recent drug called PBT2, which works by lowering amyloid-beta levels, has also shown great promise in animal studies, and has been approved for an international human clinical trial study. Both the amyloid-beta antibody therapy and PBT2 have demonstrated reductions in brain amyloid plaque burden as well as improvements in memory tasks in studies using animal models of AD.
In addition to these therapies, there are numerous other drugs and therapeutic approaches (one approach involves administering a virus that expresses nerve growth factor (NGF) in the brain—the NGF helps to repair and sustain damaged neurons) that are in human clinical studies and are showing promising results. Researchers are thus confident that it is only a matter of time before an effective treatment for AD is found.
What really happens to the brain when a person gets Alzheimer’s disease?
Alzheimer’s disease (AD) most severely affects three brain regions—the hippocampus, the temporal lobe, and the nucleus basalis of Meynert. All three play important roles in memory formation, which is why AD patients have trouble learning new facts.
On a cellular level, the two proteins most often linked to Alzheimer’s disease pathology are amyloid-beta and tau. Amyloid-beta is normally thought to play a role in neuronal development and nerve membrane repair; however, in an Alzheimer’s patient it is abnormally deposited and becomes part of neuritic plaques. These plaques form and are deposited in the space outside of brain cells and are likely toxic to the cells. Then there is the protein called tau, which normally functions to stabilize structures called microtubules in nerve cells. Microtubules are important for transporting nutrients and other substances. In AD, tau is chemically altered, and the abnormal tau molecules stick together, forming neurofibrillary tangles inside the brain’s nerve cells. Without the stabilizing help of tau, the microtubules disintegrate, transportation is disrupted, and the nerve cells eventually die. Scientists agree that neuritic plaques and neurofibrillary tangles play some role in causing the pathology of AD, such as degeneration and tissue loss in those brain areas involved in memory, as noted above.
Later in the disease, AD affects the frontal lobe, which acts as the “executive” of the brain. When the frontal lobe degenerates, the patient exhibits symptoms such as impaired judgment, poor organization and planning, distractibility, irritability, apathy, and poverty of speech.