New Study from Australia Links Benzos to dementia thru microglial cells

The article is in The Daily Mail Online, not exactly the NY Times, but it still wonderful they published this study and it is great for spreading awareness. They have found the link is through the microglial cells: which was previously unknown.

 

https://www.dailymail.co.uk/health/article-10970837/Anti-anxiety-drugs-interfere-persons-neurons-increase-risk-cognitive-decline.html

 

 

"Anti-anxiety drugs can interfere with a person's neurons and increase their risk of cognitive decline later in life, study finds:

-Researchers have discovered the reason why anti-anxiety medications put users at risk of dementia down the line

-The medications can cause damage to the brain's microglial cells - which in turn damage connects between parts of the brain

-The research team hopes their findings will open the door for a development of a new class of anxiety medication that doesn't cause brain damage

-The number of Americans using anxiety medications surged during the COVID-19 pandemic, and their use especially jumped among teens.

 

Using anti-anxiety drugs may put someone at significant risk of developing cognitive decline later in life and scientists may have finally discovered why.

 

Researchers from the Australian Nuclear Science and Technology Organisation (ANTSO) found that the drugs may impact the brain's microglial cells, which in turn interfere with the dendritic spines - a key part of the brain's neurons.

 

In essence, the drugs slowly cause impact to the part of the brain that electrifies and activates cells.

 

Millions of Americans use these drugs, and the link between them and an increased risk of cognitive decline later in life has long been known. Researchers are hopeful that their finding will open the door to a new class of drugs that have a lesser long-term impact on brain health.

'This observation is important because long-term use of anti-anxiety medication is thought to contribute to an acceleration of dementia and how that might occur was not known,' Richard Banati, a professor at ANTSO said, per Neuroscience News.

 

He explains that the brain has billions of neurons, which are electrical impulses that transmit information and send chemical signals between parts of the brain.

 

The neurons connect to one-another through a link called a synapse.

 

A majority of research on the impact of anxiety meds on cognitive decline has focused on the neurons and synapse between them.

 

Where the ANTSO team instead decided to look was the microglial cells.

 

'These are small and highly mobile cells that are part of the non-neuronal matrix in which nerve cells are embedded,' Banati explained.

 

'This matrix makes up a substantial part of the brain and is actually directly influencing the functioning of neural networks.'

 

The team tested diazepam, a common anxiety medication, to see how it would react to a neurological system in mice.

 

They found that it did not go directly to the synapses - but instead to the microglia - which is not what many experts would have expected.

 

'The drug changed the normal activity of microglial cells and indirectly the maintenance function that microglia have around synaptic nerve cell connections,' Banati explained.

 

'It is intriguing to see how the brain's local immune system, of which microglial cells are part, directly participates in the overall functional integrity of the brain.'

 

This means that the reason why some who take the medication suffer from severe fatigue - and even dementia and other cognitive issues later in life - could be because of the microglial cells.

 

Experts describe it as frying the wires in a machine. If the wires become damaged, they may work slower - if not at all.

 

Eventually if enough wires are damaged, the entire machine - which would be the brain in this case - may lose some operations all together.

 

The research is still in its early stages, but the groundbreaking findings open the door to a new class of anxiety medications that can hinder the impacts of the mental condition without causing long-term damage to the brain.

 

It comes at a welcome time as well, because the number of Americans using these medications surged during the pandemic - particularly young people.

 

Prescriptions for the drugs jumped 21 percent when the COVID-19 pandemic began, with the largest leap among those aged 13 to 19.

 

What is Alzheimer's?

 

Alzheimer's disease is a progressive, degenerative disease of the brain, in which build-up of abnormal proteins causes nerve cells to die.

 

This disrupts the transmitters that carry messages, and causes the brain to shrink.

 

More than 5 million people suffer from the disease in the US, where it is the 6th leading cause of death, and more than 1 million Britons have it.

 

WHAT HAPPENS?

 

As brain cells die, the functions they provide are lost.

 

That includes memory, orientation and the ability to think and reason.

 

The progress of the disease is slow and gradual.

 

On average, patients live five to seven years after diagnosis, but some may live for ten to 15 years.

 

EARLY SYMPTOMS:

 

Loss of short-term memory

Disorientation

Behavioral changes

Mood swings

Difficulties dealing with money or making a phone call

 

LATER SYMPTOMS:

 

Severe memory loss, forgetting close family members, familiar objects or places

Becoming anxious and frustrated over inability to make sense of the world, leading to aggressive behavior

Eventually lose ability to walk

May have problems eating

The majority will eventually need 24-hour care

 

Source: Alzheimer's Association

 

 

 

 

 

Interesting.  Below is the citation and abstract for the study referenced in the Daily Mail article.  The research subjects were ‘Gabra RRRR quadruple point-mutated mice.’

 

Shi, Y., Cui, M., Ochs, K. et al. Long-term diazepam treatment enhances microglial spine engulfment and impairs cognitive performance via the mitochondrial 18 kDa translocator protein (TSPO). Nat Neurosci 25, 317–329 (2022). https://doi.org/10.1038/s41593-022-01013-9

 

Abstract

Benzodiazepines are widely administered drugs to treat anxiety and insomnia. In addition to tolerance development and abuse liability, their chronic use may cause cognitive impairment and increase the risk for dementia. However, the mechanism by which benzodiazepines might contribute to persistent cognitive decline remains unknown. Here we report that diazepam, a widely prescribed benzodiazepine, impairs the structural plasticity of dendritic spines, causing cognitive impairment in mice. Diazepam induces these deficits via the mitochondrial 18 kDa translocator protein (TSPO), rather than classical γ-aminobutyric acid type A receptors, which alters microglial morphology, and phagocytosis of synaptic material. Collectively, our findings demonstrate a mechanism by which TSPO ligands alter synaptic plasticity and, as a consequence, cause cognitive impairment.

Thank you for linking the actual study, Libertas! I only thought of that afterwards- finding the source- but them I jumped on a group call with Jennifer Swantikowski, PhD. So happy you found it!

I was diagnosed with Memory Impairment and Amnesia many years ago and know I've got benzo-induced dementia now.  Doc wanted me to get a brain MRI and do memory testing, but I didn't.

Great idea to post this.

Now I’m very interested in learning about the function microglial cells play and possibly how to heal them, once they’ve become damaged. They are usually in an immune system role, also cleaning out neuronal waste, and pruning and shearing unused pathways. But once damaged, they can create inflammation and not do their job as they once did. I feel that brain inflammation every day. Now I just want to know everything I can as a layperson to heal those microglia. Would love to see more research!

Now I’m very interested in learning about the function microglial cells play and possibly how to heal them, once they’ve become damaged. They are usually in an immune system role, also cleaning out neuronal waste, and pruning and shearing unused pathways. But once damaged, they can create inflammation and not do their job as they once did. I feel that brain inflammation every day. Now I just want to know everything I can as a layperson to heal those microglia. Would love to see more research!

 

I feel that inflammation constantly too, and I suspected some sort of immune response being the cause of most of my symptoms. Good find this, thanks for sharing

I have a diagnosed Lupus autoimmune disease and take an aspirin or two at bedtime to reduce the inflammation.

I found the following article from 2022 that analyzes the link between the immune response and neurodegenerative disorders and the role inflamed microglia plays in all of it. It seems we really need to focus on reducing the inflammation to prevent and heal these problems. They pose that ketamine helps as an anti-inflammatory and heals synapses and the Pfizer drug Enbrel has shown much promise against Alzheimers (great, another drug-- not sure if this was debunked)- which they say reduces inflammation. Anyway, interesting article, would love to get others opinions on it, for whomever reads it.

 

https://www.statnews.com/2020/01/17/microglia-new-brain-target-depression-alzheimers-more/

I found the following article from 2022 that analyzes the link between the immune response and neurodegenerative disorders and the role inflamed microglia plays in all of it. It seems we really need to focus on reducing the inflammation to prevent and heal these problems. They pose that ketamine helps as an anti-inflammatory and heals synapses and the Pfizer drug Enbrel has shown much promise against Alzheimers (great, another drug-- not sure if this was debunked)- which they say reduces inflammation. Anyway, interesting article, would love to get others opinions on it, for whomever reads it.

 

https://www.statnews.com/2020/01/17/microglia-new-brain-target-depression-alzheimers-more/

 

Just had a quick look at that article, very interesting. I'll have a proper read a bit later.

 

I've actually been trying to reduce inflammation for a while, but like most, supplements are a bit hit and miss with me. Although it is getting better and managed to include a couple of things. I've been using a product called "clear mind" for about a week, and really seems to help.

 

https://ipothecarystore.com/products/clear-mind-dmso-nasal-spray

 

Found a paper that may be of interest to anyone that wants to reduce inflammation via the microglia

 

Inhibitors of Microglial Neurotoxicity: Focus on Natural Products

 

In recent years, many herbal plants and their active components have emerged and have been subjects of extensive research. These medications have been validated by traditional usage and are time-tested, as compared to modern day trendy supplements. The traditional herbal medicines with dependable ethnopharmacological properties have recently been demonstrated to possess neurotrophic and neuroprotective abilities, which can be useful in preventing various forms of neuronal cell loss in neurodegenerative and neuroinflammatory diseases. During the last two decades, several ingredients from natural products have been tested for their inhibitory actions on neuroinflammation and used as aids to improve memory, treat neurodegenerative diseases or create favorable effects on the CNS

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6259841/

Yes, that's a good study, especially for those of us who want to keep it natural- even though many of us cannot even take natural supplements. Myself included, though I have just started tolerating some things. Since I am far too impaired to accurately paraphrase what the study wrote on the following supplements, I shall just list them here:

 

All these have been shown in studies to have neuroprotective and anti-inflammatory properties.

 

1) Ginseng

 

2) Curcumin (active ingredient in turmeric)

 

3) Green Tea

 

4) Reservatol (found in grapes) Very promising!

 

5) Gastrodin from Gastrodia Elata

 

6) Ginger

 

7) Obovatol found in magnolia leaves

 

 

 

 

Just read that low-dose naltrexone (Ldn) inhibits microligia activation

 

Both naloxone and naltrexone have been demonstrated to exert neuroprotective and analgesic effects [22]. The neuroprotective action appears to result when microglia activation in the brain and spinal cord is inhibited

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3962576/

Well, maybe it could help but it is another drug that they are pushing. I heard that the pharma/psych has developed a new disorder for people grieving over one year and they call it "prolonged grief disorder" and guess what drug they are pushing for it? Naltrexone. They say it will stop one's "craving" for a deceased loved one. They will stop at nothing. So I am leery of using another drug to heal to heal the damage a previous drug did.

Well, maybe it could help but it is another drug that they are pushing. I heard that the pharma/psych has developed a new disorder for people grieving over one year and they call it "prolonged grief disorder" and guess what drug they are pushing for it? Naltrexone. They say it will stop one's "craving" for a deceased loved one. They will stop at nothing. So I am leery of using another drug to heal to heal the damage a previous drug did.

 

Really? That's terrible! Why not just drug everyone? Just making shit up now......

 

Yeah, I'll be sticking to natural things in the hope of speeding things up. Just thought I'd share incase anyone was looking in the future

Well, maybe it could help but it is another drug that they are pushing. I heard that the pharma/psych has developed a new disorder for people grieving over one year and they call it "prolonged grief disorder" and guess what drug they are pushing for it? Naltrexone. They say it will stop one's "craving" for a deceased loved one. They will stop at nothing. So I am leery of using another drug to heal to heal the damage a previous drug did.

 

Really? That's terrible! Why not just drug everyone? Just making shit up now......

 

Yeah, I'll be sticking to natural things in the hope of speeding things up. Just thought I'd share incase anyone was looking in the future

 

I know, right? Just put it in the water...except then they can't charge for it. I think its best to keep our remedies natural and maybe it will be a  slower process but ultimately more healthy and sustainable healing timeline.

They'll make up any disorder to put people on drugs.  Prolonged Grief Disorder?  Good Lord!  Big Pharma wants everyone to be put on psyche drugs it seems.

Well, maybe it could help but it is another drug that they are pushing. I heard that the pharma/psych has developed a new disorder for people grieving over one year and they call it "prolonged grief disorder" and guess what drug they are pushing for it? Naltrexone. They say it will stop one's "craving" for a deceased loved one. They will stop at nothing. So I am leery of using another drug to heal to heal the damage a previous drug did.

 

They are crazy.

 

Some people always feel bad about losing a loved one. It's not over in a year.

 

I don't trust psyche Drs anymore. They scare me.

 

There answer is a pill for everything.

We cannot trust anyone in the medical field again and we have to be our own biggest advocates. They have to earn our trust and we cannot just give it anymore. There is this October 2021 NY Times article that shows "Phony Diagnoses Hide High Rates of Drugging in Nursing Homes: At least 21 percent of nursing home residents are on antipsychotic drugs, a Times investigation found."

 

They use these drugs as chemical straitjackets.

 

Here's an excerpt from the article:

 

A New York Times investigation found a similar pattern of questionable diagnoses nationwide. The result: The government and the industry are obscuring the true rate of antipsychotic drug use on vulnerable residents.

 

The share of residents with a schizophrenia diagnosis has soared 70 percent since 2012, according to an analysis of Medicare data. That was the year the federal government, concerned with the overuse of antipsychotic drugs, began publicly disclosing such prescriptions by individual nursing homes.

 

Today, one in nine residents has received a schizophrenia diagnosis. In the general population, the disorder, which has strong genetic roots, afflicts roughly one in 150 people. Schizophrenia, which often causes delusions, hallucinations and dampened emotions, is almost always diagnosed before the age of 40.

 

“People don’t just wake up with schizophrenia when they are elderly,” said Dr. Michael Wasserman, a geriatrician and former nursing home executive who has become a critic of the industry. “It’s used to skirt the rules.” Some portion of the rise in schizophrenia diagnoses reflects the fact that nursing homes, like prisons, have become a refuge of last resort for people with the disorder, after large psychiatric hospitals closed decades ago.

But unfounded diagnoses are also driving the increase. In May, a report by a federal oversight agency said nearly one-third of long-term nursing home residents with schizophrenia diagnoses in 2018 had no Medicare record of being treated for the condition.

 

For nursing homes, money is on the line. High rates of antipsychotic drug use can hurt a home’s public image and the star rating it gets from the government. Medicare designed the ratings system to help patients and their families evaluate facilities using objective data; a low rating can have major financial consequences. Many facilities have found ways to hide serious problems — like inadequate staffing and haphazard care — from government audits and inspectors."

 

 

Absolutely criminal. People are dying more rapidly from the devastating consequences of these drugs, or living in deplorable health.

 

 

I think they diagnose elderly patients in nursing home as psychotic so that they can give them Seroquel or other AP's to shut them up.  I had a bf one time whose mom had dementia and they would give her Seroquel to make her be quiet.  People with dementia are known to have hallucinations because of their illness.  They aren't schizophrenic. 

You're right, Becks.