Can vitamin E slow Alzheimer’s disease (AD) progression?
According to a new double-blind, placebo-controlled trial found that alpha tocopherol (2000IU/d vitamin E) reduced the rate of functional decline in 561 patients with mild to moderate AD.
In the vitamin E group, the delay in clinical progression of AD was translated to 19% per year compared with placebo or a delay of approximately 6.2 months over the follow-up period.
… do you include VitaminE rich foods in your diet? much love.
Neurology Now (January 14, 2014)
Dysken, M.W. (2014). Journal of the American Medical Association.
Just wanted to point out that I have a new tab… RESEARCH OPPORTUNITIES.
And, yes, that means I am off-and-running with my latest research study. SO, PLEASE check it out if you are interested in getting involved – Specifically, I’m looking for care partners of persons with Alzheimer’s disease, dementia or Parkinson’s disease to fill out a questionnaire! *the 4 hours/week requirement could include basic housekeeping chores (laundry, dishes, cleaning), errands (shopping), transportation, cooking – I’m looking for people across all disease stages.
Pretty simple, and you could be doing your part to better understands unique care needs and experiences across disease groups.
… looking forward to hearing from you! much love.
The dementia themed posts this month are in honour of Alzheimer’s awareness month. If you’re interested, past posts include: defining dementia, dementia gene, G8 dementia summit, and Azheimer’s vs. Parkinson’s disease.
About 747,000 Canadians have Alzheimer’s disease and dementia and this number is expected to climb to 1.4 million in less than 20 years.
Recently, the Alzheimer’s Society Canada (ASC) is warning that 50% of Canadians with dementia are not diagnosed early enough… losing valuable time when early interventions may help manage day to day living and enable better planning for the future.
During Alzheimer’s awareness month, ASC is advising the public and healthcare professionals to spot early warning signs of dementia in family members and patients. There is often stigma associated with dementia, and people may be hesitant to share warning signs they see in themselves, such as loss of judgment or forgetfulness, to their doctors or family members.
… More info on ASC’s early diagnosis HERE. much love.
Alzheimer’s Society Canada
Global News (Carmen Chai, Jan 7/14)
Parkinson’s disease (PD) is more than a movement disorder.
Dementia is one of the things people worry about. And a number of people with PD can develop cognitive changes. I want to stress these are DIFFERENT things.
Dementia is a loss of intellectual function (memory, reason, problem solving, abstract reasoning) which is qualitatively different from a previous state of life. Dementia is chronic and progressive and impairs vocational/social function. *Remember the difference between dementia (the umbrella term) and Alzheimer’s disease (AD – a type of dementia)… read more about that HERE.
Now, AD, a type of dementia, involves the external part of the brain (the wrinkly part!), including the neocortex, and typically presents with memory/learning problems.
This is different than cognitive changes that occur in PD.
The basal ganglia part of the brain (subcortical – inner part of brain!) is affected in PD. The basal ganglia is not just involved in coordinated movement, but a junction site for some cognitive processing. So, cognitive changes in PD are a bit different – it may includes difficulty learning something, but memory of the material is retained. Cognitive changes include slowness of thought, insight, mental flexibility, attention/focus (vigilance). This is where cueing is helpful to retrieve information and for timing. We also see changes in “executive function” in PD, which basically monitors other processes; it is higher cognitive functioning that controls how we interact in the world (timing, appropriate behaviour, sequencing, tasking).
… does that start to clear these terms up? This is my current area of research focus… specifically the impact of these cognitive changes on caregivers, so lots more to come on this! much love.
Did you know the G8 health ministers met in London December 11th for a one-day summit on dementia? Mimi Lowi-Young, CEO, Alzheimer Society of Canada, along with Federal Health Minister Rona Ambrose and other leading Canadian researchers attended.
Their goal is to find an effective treatment for dementia by 2025 and improve the quality of life for people who are affected. This is an important public health problem, as dementia affects more than 35 million people worldwide and is expected to almost double every 20 years.
The ministers committed to 12 goals to address the human and economic toll of dementia-related illnesses, including “the ambition to identify a cure or a disease-modifying therapy for dementia by 2025 and to increase collectively and significantly the amount of funding for dementia research to reach that goal.” They also called for innovative ways to improve the quality of life for people with dementia and their caregivers while reducing its emotional and financial burden.
Alzheimer’s disease International
The entire document and all 12 goals can be read HERE.
Also, Canada and France will co-host a meeting in Ottawa in 2014 that will focus on partnering academia and industry to put research into practical ideas and care models. The U.K. government is also appointing a dementia team to explore a private and philanthropic fund for global dementia innovation.
Looking forward to seeing how this creates new and innovative partnerships for dementia research in 2014! much love.
A variant gene thought to play a role in Alzheimer’s disease, the ε4 allele of the gene for apolipoprotein E, may be associated with other forms of dementia (Zabetian et al, Archives of Neurology, 2012).
In this study, the researchers defined four types of dementia – Alzheimer’s without Lewy body neuropathologic changes, Lewy body disease with Alzheimer’s features, pure Lewy body disease (with low or no Alzheimer’s features), and Parkinson’s dementia (also with low or no Alzheimer’s features).
The variant – the ε4 allele of the gene for apolipoprotein E (APOE) – was elevated in both Parkinson’s and Lewy body dementia. This suggests that APOEε4 can play other roles (i.e., other than amyloid degeneration in AD) in neurodegeneration.
So, does this imply a commonality? Interesting thoughts! much love.
I want to start the new year off by clarifying some terminology around dementia.
If dementia was a “car”, Alzheimer’s disease would be a “Ford”
… meaning Alzheimer’s disease is a TYPE of dementia. Lewy Body Dementia is a TYPE of dementia.
Dementia is not a specific disease. It’s a condition in which a set of symptoms exist that cause individuals to have difficulty functioning in their daily lives. These symptoms are related to thinking and to social abilities, and can include memory loss, impaired judgment and difficulty with language.
The most common type of progressive dementia is Alzheimer’s Disease. Alzheimer’s is not a normal part of aging. Symptoms are caused by the destruction and death of nerve cells in the brain. Continued research is needed to determine exactly how and why the destruction begins. So, while Alzheimer’s is a type of dementia, not all dementias are related to Alzheimer’s. Symptoms may be similar, but it is important to obtain a thorough medical evaluation when dementia is suspected in order to determine the appropriate cause.
Lewy body dementia is another type of progressive dementia. Lewy bodies are abnormal clumps of protein in the brain that can cause tremors and rigidity similar to Parkinson’s Disease; visual hallucinations; fluctuations between confusion and clear thinking; and rapid eye movement sleep behavior disorder, in which an individual acts out dreams.
… If you’re interested in learning more about Lewy body dementias, check out this great video seminar from the LBDA Speaker’s kit “When it isn’t Alzheimer’s” HERE
. More on this to come… much love.