"Give with a free hand, but give only your own."
 -- J.R.R. Tolkien The Children of Hurin
- Anesthetics -

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Can inhaled anesthetics initiate a biochemical cascade or domino effect leading to degenerative neurological diseases? So many people have noticed a big change in their LO's mental abilities after surgery that I think there are too many clouds to believe they don't carry the rain.

Symptoms appearing after surgery seems to be a common thread in these tales. In my mother's case, the surgery was in mid 1999. We started noticing symptoms in mid 2000. Since we know that CBD progresses slowly, I think the 1 year between surgery (with inhaled anesthetic) and the development of symptoms is not out of character. It is also interesting that the first case of CBD was identified in 1968, and it was over 10 years later that other cases were reported. Is it possible that the disease, as we see it now, did not exist before this, and is being caused by exposure to a chemical? The inhaled anesthetic, halothane was introduced in 1956, and used through the 1980s. It was replaced in the 1980s by enflurane and isoflurane. [from Wikipedia]. Prior to 1956, volatile anaesthetics such as diethyl ether and cyclopropane were used.

The Inhalation Anesthetic Isoflurane Induces a Vicious Cycle of Apoptosis and Amyloid -Protein Accumulation
The Journal of Neuroscience, February 7, 2007, 27(6):1247-1254; doi:10.1523/JNEUROSCI.5320-06.2007

"... Collectively, these findings suggest that isoflurane can induce apoptosis, which, in turn, increases BACE and {gamma}-secretase levels and A secretion. Isoflurane also promotes A aggregation. Accumulation of aggregated A in the media can then promote apoptosis. The result is a vicious cycle of isoflurane-induced apoptosis, A generation and aggregation, and additional rounds of apoptosis, leading to cell death."

Molecular mechanism behind aggregation of amyloid beta peptide due to anesthetics
Medical Research News Published: Sunday, 28-Jan-2007

"Previous studies by the Pittsburgh researchers found that the inhaled anesthetics halothane and isoflurane and the intravenous anesthetic propofol encouraged the growth and clumping of Abeta in a test tube experiment."

Anesthesia Leads to Tau Hyperphosphorylation through Inhibition of Phosphatase Activity by Hypothermia
The Journal of Neuroscience, March 21, 2007, 27(12):3090-3097; doi:10.1523/JNEUROSCI.4854-06.2007

"...We found that, regardless of the anesthetic used, anesthesia induced rapid and massive hyperphosphorylation of tau, rapid and prolonged hypothermia, inhibition of Ser/Thr PP2A (protein phosphatase 2A), but no changes in APP metabolism or A (-amyloid peptide) accumulation. Reestablishing normothermia during anesthesia completely rescued tau phosphorylation to normal levels. Our results indicate that changes in tau phosphorylation were not a result of anesthesia per se, but a consequence of anesthesia-induced hypothermia, which led to inhibition of phosphatase activity and subsequent hyperphosphorylation of tau..."


Role Of Anesthetics In Alzheimer's Disease: Molecular Details Revealed

ScienceDaily (Jan. 25, 2007) Inhaled anesthetics commonly used in surgery are more likely to cause the aggregation of Alzheimer's disease-related plaques in the brain than intravenous anesthetics say University of Pittsburgh School of Medicine researchers in a journal article published in the Jan. 23 issue of Biochemistry. This is the first report using state-of-the-art nuclear magnetic resonance (NMR) spectroscopic technique to explain the detailed molecular mechanism behind the aggregation of amyloid β (Aβ) peptide due to various anesthetics...

Common Anesthetic May Induce Cell Death, Generation Of Alzheimer's-Associated Protein

ScienceDaily (Feb. 7, 2007) A new study has found how one of the most commonly used anesthetics may produce Alzheimer's-like changes in the brain. Previous studies have shown that applying the anesthetic isoflurane to cultured neural cells can lead to generation of amyloid-beta protein -- the key component of senile plaques seen in the brains of Alzheimer's patients -- and to the cell-death process known as apoptosis. In the Feb. 7 Journal of Neuroscience, researchers from Massachusetts General Hospital (MGH) and colleagues describe how isoflurane may set off a process in which A-beta generation and apoptosis interact with and magnify each other. Since this work was done in cell cultures, it is unknown whether the findings reflect a possible effect of the anesthetic on human brains...

Common Anesthetic Induces Alzheimer's-Associated Changes In Mouse Brains

ScienceDaily (Nov. 14, 2008) For the first time researchers have shown that a commonly used anesthetic can produce changes associated with Alzheimer's disease in the brains of living mammals, confirming previous laboratory studies...

Inhaled Anesthetics Accelerate Appearance Of Brain Plaque In Animals

ScienceDaily (Mar. 10, 2007) Researchers at the University of Pennsylvania's School of Medicine have discovered that common inhaled anesthetics increase the number of amyloid plaques in the brains of animals, which might accelerate the onset of neurodegenerative diseases like Alzheimer's...

Anesthesia And Alzheimer's Disease

ScienceDaily (Apr. 25, 2008) In studies of human brain cells, the widely-used anesthetic desflurane does not contribute to increased production of amyloid-beta protein; however, when combined with low oxygen conditions, it can produce more of this Alzheimer's associated protein...
Surgery Not Linked to Memory Problems in Older Patients

ScienceDaily (Nov. 19, 2009) For years, it has been widely assumed that older adults may experience memory loss and other cognitive problems following surgery. But a new study from researchers at Washington University School of Medicine in St. Louis questions those assumptions. In fact, the researchers were not able to detect any long-term cognitive declines attributable to surgery in a group of 575 patients they studied... We were able to use patients as their own controls before and after surgery and to compare groups of patients over time, and we did not detect any evidence of a long-term cognitive decline," Evers says. "Our findings suggest that if older people physically recover from surgery, they should expect that within six months or a year, they will return to their previous level of cognitive ability, too."...

Anesthesia Increases Risk of Developing Alzheimer's Disease in Patients With Genetic Predisposition, Study Suggests

ScienceDaily (Mar. 25, 2010) A new study confirms that anesthesia is safe for normal mice but potentially harmful for mice with genetic risk factors for Alzheimer's disease (AD). Over several months, investigations have focused on analyzing the effects of the anesthesia in normal mice and in mice with mutations that produce AD. The use of repetitive anesthesia with isoflurane (one of the most common anesthetics by inhalation) increases the risk of developing changes similar to those observed in AD brains in mice with mutations of the amyloid precursor protein (APP)...

Alzheimer's: Bigger Molecular-Sized Anesthetics Do Not Promote Amyloid Beta Peptide Micro-Aggregation

ScienceDaily (Apr. 20, 2010) Alzheimer's disease (AD) is a neurodegenerative disorder affecting millions of people worldwide and has become a major global concern. Uncontrolled oligomerization (aggregation) of Aβ peptide is the hallmark of AD and it is believed to be causally related to AD pathomechanism. Intensive research (biophysical, animal model and clinical) is underway to investigate the cause of this unexplained aggregation of Aβ peptide, which is probably triggered by some agent or process in predisposed individuals, and subsequently to trace the molecular pathways involved in the phenomenon.  In the April issue (Vol 20, 1, pages 127-134, 2010) of the Journal of Alzheimer's Disease, a laboratory observation based on state-of-the-art nuclear magnetic resonance spectroscopy, suggests a molecular pathway for a possible link between anesthesia and Aβ peptide aggregation. It was observed that the larger sized intravenous anesthetic diazepam (both at clinical and at very high concentration), when incubated in isolation with amyloid beta-peptide, does not promote aggregation in laboratory results monitored serially, even sixty-three days after the onset of incubation. However, if diazepam is co-incubated with halothane (a general inhaled anesthetic with small molecular size, and often used as an add-on in the clinical setting), profound amyloid beta-peptide oligomerization is observed, and the presence of the larger molecular-sized diazepam is rendered ineffective in preventing Aβ oligomerization...

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