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My grandmother, Bella, a former nurse in the Ukraine, moved to the United States to help raise me when I was 7 months old. She was diagnosed with Alzheimer’s disease last year.
There was nothing to do to prevent her inexorable loss of memory and independence, her Massachusetts General Hospital memory specialist told our family, except to take a drug called memantine that slightly improves cognition in Alzheimer’s patients, but does not treat the underlying disease.
While it is widely shown that possessing the ApoE4 gene is the major genetic risk factor of Alzheimer’s disease (AD), not all ApoE4 carriers develop AD. For the first time, researchers at Boston University School of Medicine (BUSM) have shown that ApoE4 linked with chronic inflammation dramatically increases the risk for AD. This can be detected by sequential measurements of C-reactive protein, a common clinical test which can be could be done routinely in a clinical setting.
“Finding out what mediating factors for ApoE4 increase AD risk is important for developing intervention and prevention of the disease,” explained corresponding author Wendy Qiu, MD, PhD, associate professor of psychiatry and pharmacology & experimental therapeutics at BUSM. “Since many elders have chronic low-grade inflammation after suffering from common diseases like cardiovascular diseases, diabetes, pneumonia and urinary tract infection, or after having surgeries, rigorously treating chronic systemic inflammation in ApoE4 carriers could be effective for prevention of Alzheimer’s dementia.”
USC scientists say Alzheimer’s could be diagnosed earlier if scientists focus on an early warning within the brain’s circulation system.
That’s important because researchers believe that the earlier Alzheimer’s is spotted, the better chance there is to stop or slow the disease.
“Cognitive impairment, and accumulation in the brain of the abnormal proteins amyloid and tau, are what we currently rely upon to diagnose Alzheimer’s disease, but blood-brain barrier breakdown and cerebral blood flow changes can be seen much earlier,” said Berislav Zlokovic, the Mary Hayley and Selim Zilkha Chair in Alzheimer’s Disease Research at the Keck School of Medicine of USC. “This shows why healthy blood vessels are so important for normal brain functioning.”
In a new review article in the Sept. 24 issue of Nature Neuroscience, Zlokovic and his colleagues recommend that the blood-brain barrier, or BBB, be considered an important biomarker — and potential drug target — for Alzheimer’s disease. Because Alzheimer’s is irreversible, and not fully understood, understanding the first step in the disease process is a critical step in fighting it.
IF YOU OR A LOVED ONE are experiencing epilepsy for the first time after age 65, you’re not alone. Among seniors, epilepsy is one of the top three most common neurological conditions. In fact, epilepsy starts more often in old age than in middle age, reflecting the parallel increase over time of some of its causes – such as stroke, Alzheimer’s disease and brain tumors.
Epilepsy poses special challenges for seniors. The first may be receiving the correct diagnosis. Gathering a clear description of the epileptic seizures may be difficult for seniors who live alone or in a residential care facility. Even if the seizures are witnessed or recorded on a smartphone, it may be difficult to recognize the signs, because seizures tend to look different in seniors than in younger people. They may be easily mistaken for other conditions that are common in seniors, such as stroke, dizziness and memory lapses. A neurologist can help uncover the problem and will likely perform an electroencephalogram, or EEG, and a brain MRI.
Once epilepsy is diagnosed, the next step is treatment with medication. For seniors, this also raises some special issues. As we age, our liver and kidneys become less efficient at eliminating drugs from the body, and we require lower and more frequent doses and more careful monitoring for side effects. Seniors with balance problems, fatigue, confusion, slow thinking or tremor may be especially sensitive to drug side effects. It’s important to communicate any concerns to your doctor so that the medication can be adjusted as needed to keep side effects at bay.
The use of benzodiazepines and related drugs (Z drugs) is associated with a modestly increased risk of Alzheimer’s disease, according to a recent study from the University of Eastern Finland. The risk increase was similar with both benzodiazepines and Z drugs regardless of their half-life. The results were published in Acta Psychiatrica Scandinavica.
Even though the increased risk for Alzheimer’s disease was small in this study, the threshold for prescribing benzodiazepines and related drugs should be high enough due to their several adverse effects and events, such as falls. These medications are commonly used for sleep problems, but their effectiveness for this indication diminishes over weeks or months. However, the risk of adverse events remains in longer-term use.
A common symptom among people with dementia is agitation, which can affect their and their carers’ well-being. Dementia experts conducted a new study and found the most effective means of addressing agitation.
In a paper that is now published in the journal International Psychogeriatrics, experts from several research institutions — including the University of Michigan in Ann Arbor, and Johns Hopkins University in Baltimore, MD — express their consensus on the best approaches to manage dementia-related behavioral and psychological symptoms.
More specifically, they speak of how to address states of agitation and psychosis in people with Alzheimer’s disease.
I had hoped that by now most adults in this country would have completed an advance directive for medical care and assigned someone they trusted to represent their wishes if and when they are unable to speak for themselves. Alas, at last count, barely more than one-third have done so, with the rest of Americans leaving it up to the medical profession and ill-prepared family members to decide when and how to provide life-prolonging treatments.
But even the many who, like me, have done due diligence — completed the appropriate forms, selected a health care agent and expressed their wishes to whoever may have to make medical decisions for them — may not realize that the documents typically do not cover a likely scenario for one of the leading causes of death in this country: dementia. Missing in standard documents, for example, are specific instructions about providing food and drink by hand as opposed to through a tube.
Advanced dementia, including Alzheimer’s disease, is the sixth leading cause of death overall in the United States. It is the fifth leading cause for people over 65, and the third for those over 85. Yet once the disease approaches its terminal stages, patients are unable to communicate their desires for or against life-prolonging therapies, some of which can actually make their last days more painful and hasten their demise.
Dementia with Lewy bodies has a unique genetic profile, distinct from those of Alzheimer’s disease or Parkinson’s disease, according to the first large-scale genetic study of this common type of dementia.
The genome-wide association study, conducted by a UCL-led collaboration of 65 academics in 11 countries and funded by Alzheimer’s Society and the Lewy Body Society, is published in The Lancet Neurology.
“Dementia with Lewy bodies accounts for 10-15% of dementia cases, yet our understanding of it lags beyond the more well-known Alzheimer’s disease, partly because it’s commonly misdiagnosed. Our findings clarify the disease’s distinctive genetic signature, which should, in the future, help improve clinical trials, and lead to more targeted treatments,” said the study’s lead author, Dr Jose Bras (UCL Institute of Neurology and Alzheimer’s Society senior research fellow).
Scientists drilling down to the molecular roots of Alzheimer’s disease have encountered a good news/bad news scenario. A major player is a gene called TREM2, mutations of which can substantially raise a person’s risk of the disease. The bad news is that in the early stages of the disease, high-risk TREM2 variants can hobble the immune system’s ability to protect the brain from amyloid beta, a key protein associated with Alzheimer’s.
The good news, however, according to researchers at Washington University School of Medicine in St. Louis, is that later in the disease, when the brain is dotted with toxic tangles of another Alzheimer’s protein known as tau, the absence of TREM2 protein seems to protect the brain from damage. Mice without TREM2 suffer much less brain damage than those with it.
The findings potentially make targeting the TREM2 protein as a means of preventing or treating the devastating neurodegenerative disease a little more complicated, and suggest that doctors may want to activate TREM2 early in the disease and tamp it down later.