- eliminating all simple carbohydrates, gluten and processed food from her diet, and eating more vegetables, fruits and non-farmed fish
- meditating twice a day and beginning yoga to reduce stress
- sleeping seven to eight hours per night, up from four to five
- taking melatonin, methylcobalamin, vitamin D3, fish oil and coenzyme Q10 each day
- optimizing oral hygiene using an electric flosser and electric toothbrush
- reinstating hormone replacement therapy, which had previously been discontinued
- fasting for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime
- exercising for a minimum of 30 minutes, four to six days per week
This report describes a novel, comprehensive, and personalized therapeutic program that is based on the underlying pathogenesis of Alzheimer's disease, and which involves multiple modalities designed to achieve metabolic enhancement for neurodegeneration (MEND).
An American over age 60 today has a 44 percent lower chance of developing dementia than a similar-aged person did roughly 30 years ago, the longest study of these trends in the U.S. concluded.
That the individual developed an early onset aggressive form of Alzheimer’s disease suggests a role for aluminium in disease aetiology. That the exposure to aluminium was through occupational exposure to aluminium dust suggests a prominent role for the olfactory system and lungs in the accumulation of aluminium in the brain.
We discovered and validated a set of ten lipids from peripheral blood that predicted phenoconversion to either amnestic mild cognitive impairment or Alzheimer's disease within a 2–3 year timeframe with over 90% accuracy. This biomarker panel, reflecting cell membrane integrity, may be sensitive to early neurodegeneration of preclinical Alzheimer's disease.
Elevated serum DDE (dichlorodiphenyldichloroethylene) levels are associated with an increased risk for AD (Alzheimer disease) and carriers of an APOE4 ε4 allele may be more susceptible to the effects of DDE.
Detailed interrogation of the single-nucleotide polymorphism, polygenic, and gene-based analyses resulted in no significant evidence that supported the presence of loci that increase the risk of both PD and AD.
With such striking epidemiologic examples, numerous lifestyle factors are now being taken seriously by researchers and clinicians as potential avenues for AD prevention, particularly given the current lack of disease-modifying treatments -- in other words, the lack of a cure. Couple these insights with advances in neuroimaging and other biomarker tests that allow for early disease identification, and it appears we have at least some control over our brain health. But is lifestyle modification enough to actually prevent or significantly delay AD? Will adopting healthy habits heed results, or are other factors such as genetic influences standing in the way?
Mounting evidence suggests that engaging in intellectually stimulating activity throughout life may protect against the development of Alzheimer's disease and other dementias. Professional activity may be an important determinant of mental activity.