What is Alzheimer’s Disease?
What is Alzheimer’s Disease?

What is Alzheimer’s Disease?

Published
Published February 2, 2023
Author
Skybird Stout

What is Alzheimer’s Disease?

Alzheimer's is a progressive brain disorder affecting memory, thinking, and behavior. It is the most common cause of dementia in older adults. It is characterized by losing brain cells and connections, leading to memory loss, confusion, and difficulty communicating or performing familiar tasks.
After many decades of research and development into treatments for Alzheimer’s Disease, why are they so unsuccessful?

7 Reasons Amyloid Hypothesis is Questionable

The amyloid hypothesis says that amyloid plaque buildup is the cause of Alzheimer’s Disease. This suggests that the protein forming the plaques is the cause. But some scientists don't agree.
Alzheimer’s Research Corrupted?
Alzheimer’s Research Corrupted?
  1. It does not explain why some people with amyloid plaques do not develop Alzheimer’s Disease. (1)
  1. It does not explain why Alzheimer’s Disease is more prevalent in specific populations, countries, and older adults.
  1. It does not address the role of lifestyle factors such as diet and exercise in developing the disease, such as social isolation. (6)
  1. Some studies have suggested that the accumulation of amyloid plaques may be a result rather than a cause of the disease; some people with amyloid plaques do not develop Alzheimer’s Disease. (2)
  1. In one study, people with higher levels of soluble beta-amyloid were less likely to experience cognitive decline, even if they had amyloid plaques. Conversely, lower levels were strongly linked to faster cognitive decline. (7)
  1. Environmental factors and genetic mutations may play a role in the development of Alzheimer’s Disease. (3,4)
  1. Other factors, such as neuroinflammation, oxidative stress, and mitochondrial dysfunction, are linked; tau proteins may be involved in the development of Alzheimer’s Disease. (5,8)

Glutathione and Alzheimer’s Disease

In Alzheimer's disease, there is evidence of oxidative stress and decreased energy production in the mitochondria.
Mitochondrial dysfunction is thought to play a role in the pathogenesis of Alzheimer's disease. Since mitochondria are cellular organelles responsible for producing energy and regulating cell survival, protecting cells against oxidative stress would be beneficial.
Glutathione is the master antioxidant, so raising glutathione would be a powerful strategy.
Clinically proven ways to raise glutathione are available—contact me today for further info.
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Citations

  1. Morris, G.P., Clark, I.A. & Vissel, B. Inconsistencies and Controversies Surrounding the Amyloid Hypothesis of Alzheimer's Disease. acta neuropathol commun 2, 135 (2014). https://doi.org/10.1186/s40478-014-0135-5
  1. Wang, S., Mims, P. N., Roman, R. J., & Fan, F. (2016). Is Beta-Amyloid Accumulation a Cause or Consequence of Alzheimer's Disease?. Journal of Alzheimer's parkinsonism & dementia1 (2), 007. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5555607/
  1. Killin, L. O., Starr, J. M., Shiue, I. J., & Russ, T. C. (2016). Environmental risk factors for dementia: a systematic review. BMC geriatrics16 (1), 175. https://doi.org/10.1186/s12877-016-0342-y
  1. Bekris, L. M., Yu, C. E., Bird, T. D., & Tsuang, D. W. (2010). Genetics of Alzheimer disease. Journal of geriatric psychiatry and neurology23 (4), 213–227. https://doi.org/10.1177/0891988710383571
  1. Gonzalez-Ortiz, F., Turton, M., Kac, P. R., Smirnov, D., Premi, E., Ghidoni, R., ... & Karikari, T. K. Brain-derived tau: a novel blood-based biomarker for Alzheimer’s disease-type neurodegeneration. Brain. https://doi.org/10.1093/brain/awac407
  1. Shafighi, K., Villeneuve, S., Rosa Neto, P., Badhwar, A., Poirier, J., Sharma, V., Medina, Y. I., Silveira, P. P., Dube, L., Glahn, D., & Bzdok, D. (2023). Social isolation is linked to classical risk factors of Alzheimer’s disease-related dementias. PLOS ONE18 (2), e0280471. https://doi.org/10.1371/journal.pone.0280471
  1. Sturchio, A., Dwivedi, A. K., Malm, T., Wood, M. J. A., Cilia, R., Sharma, J. S., Hill, E. J., Schneider, L. S., Graff-Radford, N. R., Mori, H., Nübling, G., El Andaloussi, S., Svenningsson, P., Ezzat, K., Espay, A. J., & Dominantly Inherited Alzheimer Consortia (DIAN) (2022). High Soluble Amyloid-β42 Predicts Normal Cognition in Amyloid-Positive Individuals with Alzheimer's Disease-Causing Mutations. Journal of Alzheimer's disease: JAD90 (1), 333–348. https://doi.org/10.3233/JAD-220808