Dr. Chauncey W. Crandall, author of Dr. Crandall’s Heart Health Report newsletter, is chief of the Cardiac Transplant Program at the world-renowned Palm Beach Cardiovascular Clinic in Palm Beach Gardens, Fla. He practices interventional, vascular, and transplant cardiology. Dr. Crandall received his post-graduate training at Yale University School of Medicine, where he also completed three years of research in the Cardiovascular Surgery Division. Dr. Crandall regularly lectures nationally and internationally on preventive cardiology, cardiology healthcare of the elderly, healing, interventional cardiology, and heart transplants. Known as the “Christian physician,” Dr. Crandall has been heralded for his values and message of hope to all his heart patients.

Tags: alzheimers | genes | apo3 | acetylcholine

Overcoming Bad Genetics

By Tuesday, 17 November 2020 04:39 PM Current | Bio | Archive

Alzheimer’s currently afflicts more than 5 million Americans, including 200,000 under the age of 65. As we age, the risk of Alzheimer’s disease grows. By 2025, the number of people 65 and older with Alzheimer’s is estimated to reach 7.1 million — a 40 percent increase in just 10 years.

Alzheimer’s is a progressive, degenerative disorder that attacks the brain’s nerve cells, or neurons, resulting in diminished memory, thinking, and language skills, as well as behavioral changes. Eventually, people lose their ability to function.

Neurons are essential because they produce a brain chemical, or neurotransmitter, called acetylcholine. Without this chemical, the connections to other brain cells are broken, killing them as well.

Two types of abnormal lesions are found in the brains of people with Alzheimer’s disease: beta amyloid plaques and neurofibrillary tangles.

Beta-amyloid plaques are sticky clumps of protein fragments and cellular material that form outside and around neurons.

Neurofibrillary tangles are insoluble, twisted fibers composed largely of a protein called tau, which builds up inside nerve cells.

Researchers are still trying to determine whether these lesions cause Alzheimer’s disease or they are simply markers for it.

While genetics plays a role in early onset Alzheimer’s disease, it is less instrumental in late-onset Alzheimer’s.

Early onset Alzheimer’s disease occurs between ages 30 and 60. It is rare, representing less than 5 percent of cases.

Symptoms of late-onset Alzheimer’s, by far the more common form, appear in people beginning in their early 60s.

The gene most involved in the disease is known as the APOE epsilon4 allele, or the e4 gene. This is the gene that substantially increases a person’s risk of developing Alzheimer’s, although the strength of the association varies.

While people who have the e4 gene are at higher risk than those who don’t, it is not certain they will develop Alzheimer’s. Research is showing that even if you have the gene, a healthy lifestyle may tip the scale in your favor.

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Two types of abnormal lesions are found in the brains of people with Alzheimer’s disease: beta amyloid plaques and neurofibrillary tangles.
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