How do you “redirect” a dementia patient who wants to “go home” or speak to someone who is no longer alive? How do you respond to a loved one who is living in a reality which isn’t yours? Here are a few tips that I posted yesterday on Defeat Dementia, a Facebook group which provides information and support to caregivers of dementia patients:
• Don’t worry about convincing her that her loved one has already passed away, but to pay attention to the emotion she is expressing.
• Sometimes it is helpful to encourage the patient to talk about her loved one. Try questions like “what did you do with your (mom) when you were little?”, “What do you want to say to your (mom)?”
• Perhaps having a photo of her loved one available that you can look at together, ask her to tell a story about her loved one, might be strategies that would satisfy her.
• If necessary, some caregivers have tried a white lie, like “Your (mother) lives someplace else now.” or “I can’t take you there today. Maybe tomorrow.”
• It’s helpful to try to stay in the patient’s reality, and the death of her loved one is no longer a part of her reality, so saying her (mother) is dead only confuses her.
Source: UCSF Memory and Aging Center
For more information, visit the Defeat Dementia website, join our Facebook Group, visit the UCSF Memory and Aging Channel on YouTube, or check out UCSF’s Memory and Aging Center website.
New research at Genentech provides a provocative theory about the cause of Alzheimer’s disease and suggests potential new targets for therapies to treat it, reports Ron Winslow in the February 19 issue of the Wall Street Journal.
The prevailing view about what causes Alzheimer’s disease is that deposits called beta amyloid accumulate in the brain, destroying nerve cells and ultimately, the patient’s memory. Now, new research shows there’s a very different way of looking at the disease.
The Genentech/Salk Institute team of researchers propose that a normal process in which excess nerve cells and nerve fibers are pruned from the brain during prenatal development is somehow reactivated in the adult brain and “hijacked” to cause the death of such cells in Alzheimer’s patients, writes Winslow.
According to Marc Tessier-Lavigne, executive vice president, research drug discovery at Genentech, the new findings offer evidence that “Alzheimer’s is not just bad luck, but rather it is the activation of a pathway that is there for development purposes.”
Genentech has identified potential drug candidates based on the findings and says that it may take many years for any potential treatment to be developed.
The research was published Thursday in the journal Nature.
NOTE: The photos of normal and dead nerve fibers above are from Dr. Tessier-Lavigne.
A new approach to delivering gene therapy to the brain to treat neurodegenerative diseases such as Alzheimer’s, was revealed in research findings published in the February 4 online edition of the Proceedings of the National Academy of Sciences.
UCSF neuroscientist Dr. Krystof Bankiewicz has developed a promising way to get nerve cells to help disperse gene therapy to targeted brain cells. He uses a technique called convection-enhanced delivery. The fluid containing the gene therapy is injected under pressure, delivered in pulses. Says Bankiewicz:
For the first time, specific regions of the cortex can be supplied with therapeutic agents by targeting defined regions of the thalamus…Translational experiments now are in progress to evaluate the potential of this unique gene delivery technology for the treatment of cortical dementias such as Alzheimer’s disease…
Bankiewicz’s research at UCSF has a strong focus on the development of practical approaches to gene and cell replacement therapies; he synthesizes several individual technologies into powerful new approaches to the treatment of such serious disease as brain cancer and neurodegenerative disorders, including Parkinson’s disease.
Source: Science Cafe
Researchers are further discovering how Parkinson’s kills brain cells. Neurologists have known for decades that Lewy bodies – clumps of aggregated proteins inside cells -appear in the brains of patients with Parkinson’s disease and other neurodegenerative diseases. The presence of these Lewy bodies points to problems in protein recycling and waste disposal which raises the question: how does disrupting those processes kill brain cells? Researchers at Emory University have a possible answer: by breaking a survival circuit called MEF2D.
In a study published yesterday in Science, the Emory researchers identified what could be an important pathway for controlling cell loss and survival in Parkinson’s disease. What this means is that further research could identify drugs that could regulate MEF2D, allowing brain cells to survive toxic stresses that impair protein recycling.
Sources: Longevity Meme, Emory University