As I savor each sip of my dark roast brew, I am delighted by a recently published article about the potentially neuroprotective effects of dark roast coffee. Canadian researchers at the Krembil Research Institute and University of Toronto compared light roast, dark roast, and decaffeinated dark roast coffee extracts on mouse model brains ridden with amyloid plaques and neurofibrillary tangles, typical of Alzheimer’s disease. Six different components within the coffee were tested for their impact on reducing the buildup of amyloid and tau proteins that comprise the plaques and tangles underlying Alzheimer’s disease.
Interestingly, caffeine, which has been touted by some as helpful to cognition, had no effect on the accumulation of amyloid and tau proteins. Rather, phenylindane, formed during the process of roasting coffee beans, was the only coffee bean component of the six tested (the others were caffeine, chlorogenic acid, quinic acid, caffeic acid, and quercetin) that inhibited both amyloid and tau proteins. This is the first report of its kind and lends support to the possibility of dark coffee roasts (both caffeinated and decaffeinated alike) protecting against the biological hallmarks of Alzheimer’s disease.
Does this mean we should all start sipping dark roasts as our miracle cure for Alzheimer’s disease? Of course, not – or, at least, not yet. Further studies are needed to better understand the role and optimal dosing of phenylindane and whether or not effects are replicated in humans. It is also important to recognize that excessive amounts of caffeine, as well as sugar and other ingredients often added to coffee, may be counter-productive. We just don’t have the data yet. But, I appreciate the scientific rigor of this study, and others like it, beginning to document the potentially positive effects of lifestyle and nutritional factors on the brain. And, as we await the findings of future studies, I will continue to enjoy moderate amounts of that ancient brew, and the darker the better!
If you are interested in learning more about the role of lifestyle factors in healthy brain aging, consider attending one of my upcoming talks, The CRCNJ Speaker’s Series, or participating in the individualized Psychoeducational Series, only offered at The CRCNJ. Contact us today for more information or to schedule your consultation.
Could Your Dark Brew Be Protecting You Against Alzheimer’s Disease?
As I savor each sip of my dark roast brew, I am delighted by a recently published article about the potentially neuroprotective effects of dark roast coffee. Canadian researchers at the Krembil Research Institute and University of Toronto compared light roast, dark roast, and decaffeinated dark roast coffee extracts on mouse model brains ridden with amyloid plaques and neurofibrillary tangles, typical of Alzheimer’s disease. Six different components within the coffee were tested for their impact on reducing the buildup of amyloid and tau proteins that comprise the plaques and tangles underlying Alzheimer’s disease.
Interestingly, caffeine, which has been touted by some as helpful to cognition, had no effect on the accumulation of amyloid and tau proteins. Rather, phenylindane, formed during the process of roasting coffee beans, was the only coffee bean component of the six tested (the others were caffeine, chlorogenic acid, quinic acid, caffeic acid, and quercetin) that inhibited both amyloid and tau proteins. This is the first report of its kind and lends support to the possibility of dark coffee roasts (both caffeinated and decaffeinated alike) protecting against the biological hallmarks of Alzheimer’s disease.
Does this mean we should all start sipping dark roasts as our miracle cure for Alzheimer’s disease? Of course, not – or, at least, not yet. Further studies are needed to better understand the role and optimal dosing of phenylindane and whether or not effects are replicated in humans. It is also important to recognize that excessive amounts of caffeine, as well as sugar and other ingredients often added to coffee, may be counter-productive. We just don’t have the data yet. But, I appreciate the scientific rigor of this study, and others like it, beginning to document the potentially positive effects of lifestyle and nutritional factors on the brain. And, as we await the findings of future studies, I will continue to enjoy moderate amounts of that ancient brew, and the darker the better!
If you are interested in learning more about the role of lifestyle factors in healthy brain aging, consider attending one of my upcoming talks, The CRCNJ Speaker’s Series, or participating in the individualized Psychoeducational Series, only offered at The CRCNJ. Contact us today for more information or to schedule your consultation.
When It’s “Not Alzheimer’s”
Several weeks ago, Ted Turner, 79-year old billionaire, CNN founder, and philanthropist, announced that he had dementia with Lewy bodies. When interviewed, he was not able to provide information about DLB, or readily recall its name, but expressed gratitude that it was “not Alzheimer’s.” Following in the footsteps of this disclosure was a recent article in The New York Times describing the proactive efforts of Laurie Scherrer, a Pennsylvania resident diagnosed with Alzheimer’s disease and frontotemporal dementia at age 55. So, what does it mean to have dementia that is not Alzheimer’s?
Dementia refers to global cognitive decline that is significant enough to interfere with daily functioning. While Alzheimer’s disease is the most common cause of dementia in people aged 65 years and older, there are numerous other causes of age-related dementia. In this regard, dementia can be thought of as a symptom which may be caused by a number of different diseases, such as dementia with Lewy bodies, frontotemporal dementia, cerebrovascular dementia, and Parkinson’s disease. Each type of dementia can be categorized by the specific changes that occur in the brain at a microscopic level. The exact symptoms evident in each person depends on the precise location of brain change as well as the unique brain circuitry of each individual, dependent on their life experiences and genetic predispositions. This is why no two people with dementia, even with the same type of dementia, have exactly the same symptoms. The brain is like real estate: it’s all about location, location, location.
Age-related dementias are not mutually exclusive. This means that just because a person has one type of dementia does not mean they can’t also have another type of dementia too. In fact, having dementia puts one at a higher risk for developing other dementias.
Knowing what type(s) of dementia a person has is important to planning, understanding symptoms and prognosis, and accessing treatment options and supportive resources. A comprehensive evaluation is the first step to proper diagnosis and treatment planning. If you are concerned about signs of cognitive decline, contact The Cognitive and Research Center of New Jersey to set up an evaluation and learn about interventions, including clinical trials and supportive resources. Time is brain. Call today.