Alzheimer’s disease undermines a series of stabilizing influences which the central nervous system has in place. Underactive lysosomes are promoted with high cortisol levels. This means there is opportunity for the brain to produce more white matter (lipids and protein) as a positive upside. On the downside this means the intracellular and extracellular transmission channels of cells are narrow because of the ante-inflammatory effects of cortisol. Lysosomes are severely hindered in this situation as they cannot clear:
1. Nucleic acids, 2. Carbohydrates, 3. Lipids, 4. Proteins. Over the years this can result in an accumulative affect (Mitochrondrial dysfunction).
Alzheimer’s disease is a progressive illness and the early symptoms when diagnosed means there is already significant damage done. This means that amyloid beta and Tau (which changes into toxic clumps) is unable to be kept and cleared by the human brain in healthy levels. Both amyloid beta and Tau have essential roles. In short & importantly Tau keeps the shape of cells so they are able to communicate with each other and amyloid beta is consistent with neural growth and repair.
Cortisol is consistently high. This is a concern as it reacts to any sort of stress. The higher the stress an appropriate equivalent response from cortisol is needed. Whatever promotes these high levels is important but it is a biomarker of this degenerative disease. Somatostatin is shown to decrease adrenocorticotropic hormone in vitro. This hormone acts on the adrenal cortex to release cortisol and androgens. Somatostatin has been found to be very low in the Alzheimer’s brain and its cerebrospinal fluid (up to 50% loss). As human beings age there is also a steady decline of somatostatin.
https://pubmed.ncbi.nlm.nih.gov/9757047/
https://pubmed.ncbi.nlm.nih.gov/23930978/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5413582/
https://myhealth.alberta.ca/Health/pages/conditions.aspx?Hwid=hw136623
https://www.nia.nih.gov/health/what-happens-brain-alzheimers-disease
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