References

- Tokey Hill
- Spinal Manipulation Techniques
- Myofascial Release
- Massage Therapy
- Spinal, visceral and extremity mobilizations
- Postural training
- Muscle energy
- Strain/Counterstrain
- Traditional modalities
- Ultra-sound
- Ionto-phoresis
- Phonophoresis
- Manual stretching and conditioning
- PNF patterns
- Isotonics
- Isometrics
- Isokinetic exercise
- Plyometrics
- Systemic conditions
- Lyme disease
- Myofascial Syndrome
- Sympathetic Dystrophy Syndrome
- TMJ dysfunction
- CABG
- Dementia
- Alzheimer’s disease
- Diabetes
- Celebrities

Alzheimer’s disease

The best thing to do once identification is seen is to go to a specialist, but in general good nutrition and cerebral stimulation as far as learning new languages, continuing your education on different topics you have never studied. Also certain supplementation is taken to aid in blood flow to the brain. The role of chiropractic and physical therapy is to keep the mind body connection together and the person painfree and joints functioning to the best of their ability.

Link of actual article is

http://www.merck.com/mrkshared/mm_geriatrics/sec5/ch40.jsp

Alzheimer's Disease

Alzheimer's disease (AD) is the most common form of dementia affecting the elderly, accounting for up to two thirds of cases. AD is increasingly common with age. The typical pathologic findings are a loss of neurons in multiple areas of the brain; senile plaques (composed of neurites, astrocytes, and glial cells surrounding an amyloid core); and neurofibrillary tangles (consisting of paired helical filaments). The specific pathophysiologic mechanism of neuronal cell loss in AD, as well as the role of plaques and tangles, is unknown. Plaques and tangles also occur in normal aging, (see page 381) but to a much lesser degree than in AD.

A protein involved in cholesterol transport, apolipoprotein E (apo E), has been genetically linked with AD. The [epsilon] 4 allele of apo E appears to be a risk factor for the disease, the [epsilon] 2 allele appears protective, and the [epsilon] 3 allele is neither associated nor protective. Persons with the [epsilon] 4 allele develop AD more commonly and at an earlier age than those without the allele. For example, [epsilon] 4 homozygotes have a > 50% risk of developing AD by age 70, whereas [epsilon] 2/ [epsilon] 3 persons have only a 12 to 14% risk by age 90. Another important genetic advance has been the localization of the [beta] -amyloid gene to chromosome 21, the same chromosome implicated in some cases of familial AD and AD due to Down syndrome. The finding that [epsilon] 4 binds to [beta] -amyloid may lead to the pathophysiology of the disease. However, none of these findings have yet affected the treatment of AD patients. Moreover, genetic testing for apo E genotype is generally not recommended for most routine cases.