Prevention Through Delay
Recent studies show that the accumulation of beta amyloid plaques in the brain, a major mechanism thought to cause Alzheimer’s disease (AD), could begin as early as 30 years before the first symptoms appear. As such, it is never too early to begin a preventative effort.
Current preventive strategies aim at reducing risk factors of Alzheimer’s disease and related disorders (ADRD) and could delay symptom onset by 3 or more years. Additionally, early detection and proper treatment of AD can slow symptom progression by another 2 to 5 years. For a typical individual who would first develop symptoms at age 74, prevention will push the onset of symptoms out to age 77 or older, and early detection and treatment will delay the onset of moderate dementia to between 88 and 91 years old. This approach means that it is possible to avoid spending your final years in a nursing home, to preserve your memories and abilities, and to live out your life with independence and dignity.
Symptoms and Progression
Alzheimer’s disease (AD) is a progressive disease, such that it starts in one part of the brain and slowly spreads to other parts of the brain. During the mild cognitive impairment (MCI) stage of the disease, impairment is limited to the part of the brain responsible for short-term memory. As the disease progresses, it spreads throughout the brain and impairs additional brain lobes and the functions associated with those lobes.
Progression of Alzheimer's and Symptoms
Research shows that it is possible to delay the onset and progression of Alzheimer’s disease and related disorders (ADRD) by up to several years. Given that the average age of onset is 74, a six-year delay in symptoms could keep memory intact until after age 80. Since the average life expectancy in the USA is about 78 years, this means that those who pursue an appropriate prevention strategy may never develop the symptoms of ADRD during their lifetime.
If you notice changes in memory or other cognitive functions in yourself or in others, professional evaluation and treatment should be sought immediately.
- Find the Right Physician
- Get Tested Professionally
- Collect Patient and Family History
For evaluating and treating ADRD, there is no substitute for experience and proper training. Neurologists, psychiatrists, or geriatricians are the specialists most likely to have been trained to evaluate ADRD using the NINDS-ADRDS criteria, and effectively treat the cause. Some internists or primary care physicians have also been properly trained. If you don’t know where to start, ask your primary care doctor or look up the local chapter of the Alzheimer’s Association by searching on www.alz.org.
Objective tests of mental abilities are used to confirm cognitive impairment as well as to help diagnose its cause. Of the cognitive functions impaired in Alzheimer’s Disease, short-term memory loss is one of the first. Therefore tests of short term memory loss can identify Alzheimer’s Disease at its earliest stages. Your physician or a neuropsychologist may be able to conduct such professional testing.
The medical and family history is key to a proper diagnosis of ADRD. A proper history includes:
- All medications, including over the counter medications, along with when they were started
- Past medical conditions
- List of all current medical conditions
- Life style history including head injuries, alcohol, smoking, exercise, diet, hobbies or pastimes
- Psychosocial history such as marital state, living conditions
- Family history of memory/cognitive impairment, senility/dementia, AD, ADRD and risk factors for ADRD
Treatable medical conditions that can cause cognitive impairment or dementia include diseases of virtually every organ and tissue of the body, especially the heart, lung, thyroid, kidney, liver, blood vessels and immune system. Psychiatric or neurologic conditions, such as depression, manic-depression, anxiety and stress can also affect memory and other cognitive abilities. These conditions are identified through history and physical examination, plus diagnostic tests of blood, urine, X-rays, and brain imaging.
Brain imaging has two primary functions. First, it helps establish how much damage to the brain has occurred. Second, it helps diagnose the underlying cause of the damage. The choice of which brain image to do (CT, MRI, SPECT, PET or fMRI) depends upon the duration and severity of the condition. When MRI or CT scans show no brain tissue loss, imaging of the brain’s activity should be done with SPECT, PET or fMRI to detect abnormalities and help make an early diagnosis.
Based on the history, examination, laboratory and brain imaging results, a properly trained physician can diagnose the cause of your condition with 90% accuracy or higher using NINDS-ADRDS criteria. Typically it takes a few weeks to complete a diagnostic evaluation of ADRD.
Contrary to a general belief that AD treatment does not work, currently available mediations for Alzheimer’s disease (AD) are beneficial and, in many cases, delay disease progression for 2 to 4.5 years. Combining these pharmacologic treatments with other types of treatments brings the maximum benefits to the patients. Other types of treatment include:
- Over-the-counter medications and supplements
- Cognitive, occupational and speech therapies
- Life style modifications (e.g. mental and physical exercise, and healthier diet)
- Caregiver education and social support
Today there are five FDA-approved medications for treatment of AD (e.g. Cognex (tacrine), Aricept (donepezil), Razzadyne (galantamine), Exelon (rivastigmine) and Namenda (memantine)) and all of them have shown positive treatment outcomes in long-term studies.
Cognex, Aricept, Razzadyne and Exelon belong to a class of medications called cholinesterase Inhibitors. Cholinesterase inhibitors increase the availability of acetylcholine, an important transmitter that helps control mood, behavior, memory and other cognitive abilities. Acetylcholine is markedly reduced in AD, Parkinson’s disease, Lewy body disease and many other dementing disorders.
Cholinesterase inhibitors also appear to slow the production of beta amyloid (the primary cause of AD), which delays AD progression.
Glutamate Receptor Modulators
Namenda belongs to a class of medication called glutamate receptor modulators. Glutamate is the transmitter for 75% of all neurons in the gray matter on the surface of the brain (cerebral cortex). Excessive amounts of glutamate are released in a wide variety of brain disorders, including stroke, Parkinson’s disease, multiple sclerosis, traumatic brain injury, and probably AD. The excessive release of glutamate triggers certain suicide genes in neurons to cause their self-destruction. Namenda blocks this self destruction plus allows normally released amounts of glutamate to exert their proper function in brain communication. Namenda may also block neurofibrillary tangle formation (a hallmark of AD pathology) to delay AD progression.