What can we do to prevent Alzheimer’s disease?

Close-up Of A Person's Hand Holding Ribbon With Hope Text To Support Alzheimer's Disease AwarenessDementia or “memory loss” is a term familiar to all of us. Dementias are subdivided on the basis of their underlying pathology, largely defined by accumulation of specific types of abnormal protein in the brain cells. An accurate number of individuals affected by dementia is difficult to estimate secondary to diagnostic challenges and absence of confirmation in many suspected cases.

Dementia from Alzheimer’s disease (AD) was first identified in 1906 and globally accounts for approximately 60 percent of all dementias. Estimates vary, but experts suggest that more than 5.5 million Americans, most of them age 65 or older, may have dementia caused by AD.

Those having a family member or providing health care to those with a diagnosis of AD may be familiar with the disease process; realizing how painful it can be at times to see your loved ones suffering and, in worst case, stop recognizing you. AD can have substantial consequences for patients, their families, and society in terms of morbidity, mortality, and healthcare costs.

A diagnosis of AD is suggested by insidious onset and gradual progression in two or more cognitive domains, one being memory.

Memory impairment is the essential and earliest clinical manifestation of AD. Declarative memory (facts and events) is significantly affected in AD. Specifically, episodic memory (specific events and contexts) is the most impaired in early AD. Within episodic memory, memory for recent events is more prominently impaired in early AD compared with immediate or remote memory. Memory for facts such as vocabulary and concepts (semantic memory) may be spared until later. Likewise, procedural memory and motor learning are also spared in the early stages.

Loss of visuospatial skills is also often an early feature of AD which manifests as navigational difficulty in unfamiliar and later familiar areas and misplacement of items. Other features often associated with later stages of AD include progressive language dysfunction, impaired executive function, lack of insight, neuropsychiatric symptoms, and apraxia. Inability to recognize objects and faces, or visual agnosia and prosopagnosia, respectively, are late features.

We don’t yet fully understand what causes AD in most people. In people with early-onset AD, a genetic mutation may be the cause. However, only a small percent of cases of Alzheimer’s disease are caused by a gene. Late-onset AD arises from a complex series of brain changes that occur over decades. The causes probably include a combination of genetic, environmental, and lifestyle factors.

Recently, evidence of pathological alterations in the brain tissue has been gathered, showing that the signs of brain damage appear more than 20 years before the onset of dementia from AD. Keeping this in mind, AD may be a disorder that develops over a lifetime, with individualized ways to maintain a better brain as we age.

Research has extensively shown that healthy lifestyle choices may potentially reduce the risk of developing dementia. Studies have determined that the risk of developing AD may be reduced by approximately 60 percent in study participants who adopted the following lifestyle factors which includes:

Physical Activity
Pooling of data from different studies has demonstrated that physical activity is inversely associated with the risk of AD. A study performed in 2017 showed leisure-time physical activity to be particularly protective against AD, but not work-related physical activity.

Smoking
Overall, literature indicates that former/active smoking is related to a significantly increased risk for AD. Cigarette smoke/smoking is associated with AD pathology in preclinical models and humans.

Engagement in cognitively stimulating activities
Consistent studies have shown that frequent participation in cognitively stimulating activities over the course of a lifetime is associated with reduced risk of AD Dementia.

Low Carbohydrate and Fiber Rich Foods
In a large meta-analysis 50 of the 64 reviewed studies revealed a protective effect of a high fiber diet found in fruit and vegetables, offering promising implications for diet being a modifiable risk factor for AD.

Light to Moderate Alcohol Intake
Limited studies have shown light to moderate alcohol intake being a protective factor against development of AD.

In addition, several studies investigating whether the adoption of these healthy lifestyle factors could possibly have an impact on individuals with a high genetic risk of dementia have also shown promising results.

Even though AD cannot be completely avoided with new evidence shows that the risk can be reduced to half by adopting healthy lifestyle modifications. This is encouraging, since we cannot change our genetic predisposition for the disease but by adopting a healthy lifestyle, we may reduce the risk of developing AD.

Led by Robert P. Friedland, who has authored many papers on Alzhiemer’s disease, the team of providers at UofL Physicians – Memory and Alzheimer’s Center works together to provide the best care possible for patients with conditions affecting memory and cognition.

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About Robert P. Friedland, M.D.

Dr. Friedland is a clinical and research neurologist devoted to the study of brain disorders associated with aging. He is a graduate of the City College of New York and graduated received his MD degree from the Mount Sinai School of Medicine in New York in 1973. He completed his neurology residency at the Mount Sinai Hospital and was a fellow in dementia and aging at the Albert Einstein College of Medicine, N.Y. with Robert Katzman. He then worked at the University of California, Davis, and in the Research Medicine Group of the Lawrence Berkeley Laboratory of the University California, Berkeley where he served as Chief Neurologist. From 1985 to 1990 he was Deputy Clinical Director and Chief of the Section on Brain Aging and Dementia of the National Institute on Aging, National Institutes of Health of Bethesda, Md. At the CWRU School of Medicine he was Professor of Neurology, Radiology and Psychiatry and Chief of the Laboratory of Neurogeriatrics from 1990 to 2008. In December of 2008 he joined the faculty of the University of Louisville, as the Rudd Professor and Chair of the Dept. of Neurology. Dr. Friedland’s work has focused on clinical and biological issues in Alzheimer’s disease and related disorders. Dr. Friedland has authored or coauthored over 220 scientific publications in referred journals and has received research funding from the National Institutes of Health as well as several foundations, institutes, corporations, and families. He received over $1M annual research funding to support his work from 1985-2013. He is currently on sabbatical leave in Kyoto Japan as a Long-Term Invitational Fellow, supported by a grant from the Japan Society for the Promotion of Science. He is working with collaborators at the Kyoto Prefectural University of Medicine and the Kyoto Institute of Technology on the influence of the microbiota on the development of neurodegeneration in transgenic Drosophila.

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