Susan Greenfield T14 peptide

[barbigrandm]

Hi all , recently I've read an article of Susan Greenfield asserting they have the key to reverse neuro degenerative disease. A test will be ready in six months, the treatment in 2 years. I haven't read any about that in this forum , nor to dr Dale Bredesen. ....surprisingly for me. Maybe it's well known around. Any insight?

[TheresaB]

Hi all , recently I've read an article of Susan Greenfield asserting they have the key to reverse neuro degenerative disease. A test will be ready in six months, the treatment in 2 years. I haven't read any about that in this forum , nor to dr Dale Bredesen. ....surprisingly for me. Maybe it's well known around. Any insight?

Haven't heard anything about this, so share the article or summarize the information on this.

[Tincup]

Hi all , recently I've read an article of Susan Greenfield asserting they have the key to reverse neuro degenerative disease. A test will be ready in six months, the treatment in 2 years. I haven't read any about that in this forum , nor to dr Dale Bredesen. ....surprisingly for me. Maybe it's well known around. Any insight?

Haven't heard anything about this, so share the article or summarize the information on this.

Oxidative Stress Triggers a Pivotal Peptide Linked to Alzheimer's Disease

Evidence for a novel neuronal mechanism driving Alzheimer's disease, upstream of amyloid
From the immediately above link:
"Conflict of interest statement
S.G. is the founder and CEO of Neuro-Bio Ltd. and holds all shares in the company. S.G.-R. and K.M. are employees of Neuro-Bio Ltd. N.E. is a full-time university student and completed a placement at Neuro-Bio Ltd."

From 2023:
https://www.sciencedirect.com/science/a ... 2223012969
https://pubmed.ncbi.nlm.nih.gov/37373106/

**T14** is a 14-amino-acid peptide derived from the C-terminus of acetylcholinesterase (AChE). Research led by Professor Baroness Susan Greenfield has identified T14 as a bioactive molecule that, while promoting cell growth and renewal during development, may contribute to neurodegenerative processes in adulthood when aberrantly activated.

**Role in Neurodegeneration:**
In the mature brain, inappropriate activation of T14 can lead to excessive calcium influx through the α7 nicotinic acetylcholine receptor (α7 nAChR), resulting in excitotoxicity and neuronal damage. Elevated levels of T14 have been observed in the pre-symptomatic stages of Alzheimer's disease (AD), suggesting its involvement in the early phases of neurodegeneration.

**Therapeutic Developments:**
Building on these findings, Neuro-Bio Ltd., founded by Professor Greenfield, has developed **NBP14**, a cyclized form of T14 designed to block the peptide's neurotoxic effects. Preclinical studies have demonstrated that NBP14 can reduce amyloid production and improve cognitive performance in mouse models of AD, indicating its potential as a therapeutic agent.

**Implications for Skin Aging:**
Beyond neurodegeneration, T14 has been implicated in skin aging. Studies have detected T14 immunoreactivity in human keratinocytes, with levels inversely related to age and more pronounced reductions observed with chronic photo-exposure. This suggests that T14 may play a role in skin cell growth and renewal, and its decline could contribute to the aging process.

In summary, T14 is a peptide with significant roles in both neural and skin cell biology. While it supports cell growth during development, its dysregulation in adulthood is associated with neurodegenerative diseases and skin aging. Ongoing research aims to harness this knowledge for therapeutic interventions in conditions like Alzheimer's disease.

Asked for sources from Chat GPT4

**T14 Peptide and Its Implications in Neurodegeneration and Skin Aging**

**1. T14 Peptide in Neurodegeneration**

- **Origin and Function**: T14 is a 14-amino-acid peptide derived from the C-terminus of acetylcholinesterase (AChE). It enhances calcium influx by binding to an allosteric site on the α7 nicotinic acetylcholine receptor (α7 nAChR), promoting cell growth during development.

- **Pathological Role**: In the adult brain, aberrant activation of T14 can lead to excessive calcium entry, resulting in excitotoxicity and neuronal damage. Elevated levels of T14 have been observed in the pre-symptomatic stages of Alzheimer's disease (AD), suggesting its involvement in early neurodegenerative processes.

- **Therapeutic Developments**: Neuro-Bio Ltd., founded by Professor Susan Greenfield, has developed NBP14, a cyclized form of T14 designed to block its neurotoxic effects. Preclinical studies indicate that NBP14 can reduce amyloid production and improve cognitive performance in mouse models of AD, highlighting its potential as a therapeutic agent.

**2. T14 Peptide in Skin Aging**

- **Expression in Skin**: T14 immunoreactivity has been detected in human keratinocytes, with levels inversely related to age. This decrease is more pronounced with chronic photo-exposure, indicating a potential role in skin cell growth and renewal.

- **Implications**: The decline of T14 in aging and photo-aged skin suggests its involvement in the aging process. Monitoring keratinocyte T14 levels could provide insights into the link between degenerative diseases and epidermal cell profiles.

**References**:

1. Rocha, S., et al. "A novel peptide 'T14' reflects age and photo-aging in human skin." *Aging* 15.12 (2023): 5279-5289.

2. Garcia-Ratés, S., and Greenfield, S. "When a trophic process turns toxic: Alzheimer’s disease as an aberrant recapitulation of a developmental mechanism." *International Journal of Biochemistry and Cell Biology* 149 (2022): 106260.

3. Neuro-Bio Ltd. "Novel Drug from Neuro-Bio effective in a mouse model of Alzheimer's disease." (2022).

4. Greenfield, S. "Susan Greenfield speaking at OBN's BioTuesday." Neuro-Bio Ltd. (2022).

5. Medical Xpress. "Researchers examine evidence for a novel neuronal mechanism driving Alzheimer's disease." (2024).

These sources provide detailed insights into the role of T14 in neurodegeneration and skin aging, as well as ongoing therapeutic developments targeting this peptide.

[barbigrandm]

Thank you tincup . I read the news in a newspaper of Barcelona, Spain, where she works on her research with Vall d'Hebron Hospital. Then I used the Web to keep searching. Like this video where she explain her approach. I am not scientist and is hard for me to understand whether this search line is based on beta amiloide theory or goes beyond. I have written dr Bredesen on fb but doubt it will reach to him. He would clear it up. ...........hopefully.
https://www.google.com/url?sa=t&source= ... ZSLSUetUf9

[NF52]

Thank you tincup . I read the news in a newspaper of Barcelona, Spain, where she works on her research with Vall d'Hebron Hospital. Then I used the Web to keep searching. Like this video where she explain her approach. I am not scientist and is hard for me to understand whether this search line is based on beta amiloide theory or goes beyond. I have written dr Bredesen on fb but doubt it will reach to him. He would clear it up. ...........hopefully.
https://www.google.com/url?sa=t&source= ... ZSLSUetUf9

Preclinical studies have demonstrated that NBP14 can reduce amyloid production and improve cognitive performance in mouse models of AD, indicating its potential as a therapeutic agent.

The above quote, from the article Tincup provided, does show that this is an approach to remove amyloid from the brain of mice who have been genetically engineered to develop amyloid in their brains.

The term "preclinical", as it is used here, means it is early-stage research seeking to show an effect in a model of Alzheimer's (the mouse). The next type of "test" for a drug or treatment would be a Phase 1 study in a small number of people (usually a few dozen) with confirmed Alzheimer's dementia and confirmed amyloid plaques, to see if the drug is safe and effective, with people assigned randomly to either the drug or placebo and neither the people nor the researchers knowing which is getting the drug. It would likely be years and require a large pharmaceutical company to buy this company or the drug to fund a large clinical trial, which can cost many millions of dollars.

[Tincup]

The above quote, from the article Tincup provided, does show that this is an approach to remove amyloid from the brain of mice who have been genetically engineered to develop amyloid in their brains.

From watching the video of Baroness Greenfield that barbigrandm posted above, I heard her say that they consider the lower amyloid as a downstream effect of the peptide action. Meaning less amyloid is produced rather than the peptide actually removes the amyloid. At least this is my understanding.

[barbigrandm]

https://alz-journals.onlinelibrary.wile ... /alz.13869

Here we can read that "This perspective offers an alternative to the amyloid hypothesis in the etiology of Alzheimer's disease (AD)".........Hence it should be a new approach. They are also aware of the multifactorial trigger of the disease:

"Alzheimer's disease (AD) has been the subject of intense research for decades, primarily with a focus on the β-amyloid hypothesis, in which β-amyloid accumulation initiates a cascade of neurodegeneration leading to the characteristic symptoms of memory loss, cognitive impairment and confusion. The presence of this marker is a major factor in the formal diagnosis of AD (https://www.nia.nih.gov/health/alzheime ... guidelines). However, the β-amyloid pathological cascade itself, and closely associated changes, are recognized as highly complex, involving multiple mechanisms including tau phosphorylation, defective mitochondrial function, ionic imbalances, dysfunctional autophagy, synaptic loss, neuroinflammation and impaired brain energy metabolism.1

This Perspective presents an alternative approach where we discuss a possible mechanism upstream of this multifactorial, but familiar, scenario and consider the properties of the interconnecting subcortical cell groups that have been increasingly recognized as the first to degenerate at the start of AD.2, 3 Identification of the features that differentiate these neurons from the rest of the brain could provide valuable insight into the basic process underlying AD, and point the way to an eventual means of preventing the β-amyloid cascade from being initiated..

[TheresaB]

Meaning less amyloid is produced rather than the peptide actually removes the amyloid. At least this is my understanding.

That would be great news. My crude analogy has always been that when you have a cold, you can blow your nose and feel better, but that doesn't get to the root cause of the issue. I'm thinking same can be said about removing amyloid.

However, my enthusiasm on this news is tempered in remembering how blacks and hispanics have been underrepresented in amyloid removing drug clinical trials because they have less amyloid accumulation despite having higher rates of dementia.

One Neurological Factor Keeps Black, Hispanic Patients From Alzheimer's Clinical Trials (US News and World Report April 19, 2024)

Black and Hispanic patients with Alzheimer’s disease are greatly underrepresented in clinical trials, even though they’re more likely to get dementia than whites. ...

Instead, Black and Hispanic people are being judged ineligible for Alzheimer’s trials because they appear to have lower levels of brain amyloid buildup in the early stages of the disease, researchers reported April 17 in the journal Alzheimer’s & Dementia. ...

But this study shows that more than just amyloid may be responsible for Alzheimer’s and other dementias.

[barbigrandm]

Hi again. I have found this recent interview to Susan Greenfield, where she explains quite well many questions we all might have concerning her new approach. She explains it in an easy way, so lay people (in terms of science) can understand. However, if any of you could summarize it, that would be great so we could share the core of it with others more easily . I am language limited. Thank you.