Fluoroquinolones and Alzheimer’s

How could the fluoroquinolones cause Alzheimer’s?

Fluoroquinolones Oxidative Stress Mitochondrial Dysfunction Alzheimer’s

An internal FDA pharmacovigilance review memo dated April 17, 2013 on the Fluoroquinolones (FQs), issued by the Food and Drug Administration’s Center for Drug Evaluation and Research, Office of Surveillance and Epidemiology shows that the FDA is fully aware of permanent disabling peripheral neuropathy in otherwise healthy individuals and that the likely method of action (or damage) for the peripheral neuropathy is mitochondrial toxicity. They go on to note that the method of damage, mitochondrial toxicity, is also the underlying mechanisms in neurodegenerative diseases such as Parkinson’s, Alzheimer’s, and ALS (1)

FQ’s induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells (2).

Researchers Swerdlow and Kan in 2006, state that mitochondrial dysfunction is the primary pathologic event in Alzheimer’s disease which then leads to beta-amyloid plaque deposition, synaptic degeneration, and neurofibrillary tangle formation.  While the formation of beta-amyloid plaques in brain cells is currently the prevailing hypothesis for how Alzheimer’s disease develops, oxidative damage with a subsequent decline in the brain cell’s ability to produce adequate energy (ATP), is currently being investigated as a preliminary step which leads to the formation of beta-amyloid plaques.  This is referred to as the mitochondrial cascade hypothesis (3).

The mitochondrial cascade hypothesis, as first described by researchers Swerdlow and Kan in 2006, states that mitochondrial dysfunction is the primary pathologic event in Alzheimer’s disease which then leads to beta-amyloid plaque deposition, synaptic degeneration, and neurofibrillary tangle formation.

Compelling evidence shows that the brain cells of patients with Alzheimer’s disease have an impaired ability to generate sufficient energy due to mitochondrial dysfunction, that this deficiency appears early in the clinical evolution of the disease, that it worsens with the progression of the illness, and that it may be occurring prior to the occurrence of any symptoms. Mitochondrial dysfunction is now believed by many to predate the formation beta-amyloid plaques (4).

It is important to note that not everyone that takes or has an adverse event to the FQ’s will go on to develop Alzheimer’s.  Even despite the fact that the FDA documents a neurodegenerative link, more tracking and research are needed to further elucidate the long term impact that the FQ’s are having in the causative factors of neurodegenerative disease and on society as a whole.  Given these facts, it is both prudent and wise that the very powerful fluorquinolones are used in an extremely judicious manner by medical personnel.

Further Reading:

The Role of Oxidative Stress-Induced Epigenetic Alterations in Amyloid-β Production in Alzheimer’s Disease.

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