Chemical Grows Brain Cells?


Senior Member
Chemical Grows Brain Cells?

(Ivanhoe Newswire) -- It sounds like science-fiction, but researchers have identified a chemical that causes brain cells to grow.

Investigators from the University of Texas Southwestern say the substance -- known as P7C3 -- can actually make new neurons grow. They came to this conclusion after infusing 1,000 different chemicals into the brains of live mice.

"We really didn't know if the screen would turn up a favorable compound or not," Steven McKnight, from the University of Texas Southwestern, was quoted as saying. "It was blind luck."

The researchers used P7C3 in mice that were carrying a mutation, making them incapable of producing new neurons in a specific region of the brain. Not only did new neurons form, but the scientists say electrophysiological readings showed that processing in parts of the brain were restored.

"Sure enough, we had evidence that you can actually create new neurons that work," McKnight said.

Continuous treatment with P7C3 also enhanced the birth of new neurons in the animals. The investigators say their discovery could pave the way for potential new treatments for people with Alzheimer's or other neurodegenerative diseases.

SOURCE: Cell, July 9, 2010


Senior Member
Chemical Makes Brain Cells Grow, Thwarts Mental Decline in Aging Rats
ScienceDaily (July 8, 2010) Scientists have discovered a compound that restores the capacity to form new memories in aging rats, likely by improving the survival of newborn neurons in the brain's memory hub. The research has turned up clues to a neuroprotective mechanism that could lead to a treatment for Alzheimer's disease.

"This neuroprotective compound, called P7C3, holds special promise because of its medication-friendly properties," explained Steven McKnight, Ph.D., who co-led the research with Andrew Pieper, M.D., Ph.D., both of University of Texas Southwestern Medical Center, Dallas. "It can be taken orally, crosses the blood-brain barrier with long-lasting effects, and is safely tolerated by mice during many stages of development."

The researchers report on their findings July 9, 2010 in the journal Cell. Their work was funded, in part, by the NIH's National Institute of Mental Health (NIMH), a NIH Director's Pioneer Award funded through the Common Fund and managed by the National Institute of General Medical Sciences, and National Cancer Institute.

"This striking demonstration of a treatment that stems age-related cognitive decline in living animals points the way to potential development of the first cures that will address the core illness process in Alzheimer's disease," said NIMH Director Thomas Insel, M.D.

Physical activity, social, or other enriching experiences promote neurogenesis -- the birth and maturation of new neurons. This growth takes place in the dentate gyrus, a key area of the brain's memory hub, the hippocampus. But even in the normal adult brain, most of these newborn neurons die during the month it takes to develop and get wired into brain circuitry. To survive, the cells must run a gauntlet of challenges. Newborn hippocampus neurons fare much worse in aging-related disorders like Alzheimer's, marked by runaway cell death.

In hopes of finding compounds that might protect such vulnerable neurons during this process, Pieper, McKnight and colleagues tested more than 1000 small molecules in living mice. One of the compounds, designated P7C3, corrected deficits in the brains of adult mice engineered to lack a gene required for the survival of newborn neurons in the hippocampus. Giving P7C3 to the mice reduced programmed death of newborn cells -- normalizing stunted growth of branch-like neuronal extensions and thickening an abnormally thin layer of cells by 40 percent. Among clues to the mechanism by which P7C3 works, the researchers discovered that it protects the integrity of machinery for maintaining a cell's energy level.

To find out if P7C3 could similarly stem aging-associated neuronal death and cognitive decline, the researchers gave the compound to aged rats. Rodents treated with P7C3 for two months significantly outperformed their placebo-treated peers on a water maze task, a standard assay of hippocampus-dependent learning. This was traced to a threefold higher-than-normal level of newborn neurons in the dentate gyrus of the treated animals. Rats were used instead of mice for this phase of the study because the genetically engineered mice could not swim.

Prolonged treatment of aged rats with P7C3 also enhanced the birth of new neurons. "Aged rats normally show a decline in neurogenesis associated with an inability to form new memories and learn tasks," Pieper explained.

In their study, rats treated with P7C3 each day showed evidence of an increase in the formation of newborn neurons and significant improvements in their ability to swim to the location of a missing platform, a standardized test of learning and memory in rats.

The key to the treatment's success is the protection of newborn neurons, the researchers report. In fact, they explained, the normal process by which newborn neurons are incorporated into the brain as mature cells is a long and perilous one.

"It takes a long time -- two to four weeks -- from the birth of a new neuron until it becomes functional," McKnight said. "Most of them die along the way." P7C3 essentially seems to give newborn neurons better odds.

Notably, they say that two other drugs (Dimebon and Serono compounds) -- both of which bear structural similarities to P7C3 -also encourage the growth of new neurons. It's tempting to think that all three compounds work in the same way.

The researchers pinpointed a derivative of P7C3, called A20, which is even more protective than the parent compound. They also produced evidence suggesting that two other neuroprotective compounds eyed as possible Alzheimer's cures may work through the same mechanism as P7C3. The A20 derivative proved 300 times more potent than one of these compounds currently in clinical trials for Alzheimer's disease. This suggested that even more potent neuroprotective agents could potentially be discovered using the same methods. Following up on these leads, the researchers are now searching for the molecular target of P7C3 -- key to discovering the underlying neuroprotective mechanism.


Senior Member
amazing stuff. Thanks for the links.

Thanks for your feedback Esther... here is some further info about P7C3 ......

Quote "Notably, they say that two other drugs (Dimebon and Serono compounds) -- both of which bear structural similarities to P7C3 -also encourage the growth of new neurons. It's tempting to think that all three compounds work in the same way."

Name: Dimebon

Other Names: 3,6-dimethyl-9-(2-methyl-pyridyl-5)-ethyl-1,2,3,4-tetrahydro--carboline dihydrochloride, Dimebolin, Latrepirdine, Pf-01913539

Therapeutic Applications: Approved in 1983 as an antihistamine in Russia

Therapy Types: Small molecule with a broad and pleiotropic spectrum of pharmacological properties.

Mechanisms: Has activity as an inhibitor of cholinesterase and NMDA receptors. Inhibits neuronal death, potentially by mitochondrial-mediated inhibition of apoptosis.

Development Status: investigational in U.S.
FDA Phase: Phase III
Primary Medical Role: Dimebon was initially characterized as an antagonist to H1- histamine receptor, and has been an approved antihistamine in Russia since 1983.

Role in Alzheimer's Disease: As a cognitive enhancer, Dimebon has shown efficacy in all measures of cognition and behavior in mild-to-moderate Alzheimer Disease patients. Phase II clinical trial results ( NCT00377715) have been reported (Doody et al, 2008). Treatment with dimebon resulted in significant benefits in ADAS-cog compared with placebo at week 26 (p<0.0001). Patients given dimebon were significantly improved over baseline for ADAS-cog (p=0.0005).

In vitro Dimebon protected primary neuron cultures against A toxicity (EC50=25 M) and inhibits both acetylcholinesterase (I50=42 M) and butyrylcholinesterase (IC50=7.9 M), as well as inhibiting NMDA receptors (IC50 range of 10-70 M) (Bachurin et al., 2001; Grigoriev et al., 2003). Neuroprotective effects of Dimebon has also been observed in a transgenic Drosophila model of Huntington Disease, protecting photoreceptor neurons against death induced by human Huntington protein (htt) (unpublished data, Medivation disclosure).

In a recent clinical trial in mild-to-moderate AD in Russia (completed summer 2006), Dimebon demonstrated positive clinical efficacy in cognition and behavior using five independent measures of cognitive impairment.

Pharmacological Role: Dimebon inhibits cholinesterases, the NMDA receptor and reduces mitochondrial swelling induced by A (Bachurin et al., 2003) consistent with the suggestion that Dimebon acts to block mitochondrial permeability transition pores.



XMRV+ Member
Ontario, Canada
Here's an possibly related "breakthrough" from an Alberta University
" Scientists at the University of Lethbridge say they have successfully regrown adult brain cells in tests on mice, a breakthrough that could lead to treatment of neural diseases such as Alzheimer's."
" "We discovered the memory disorder [in the mice] was reversed," Sutherland said. "It was gone. The memory was as good as normal."
Could be hopeful news for all of us with fuzzy brain. Step #1 Kill Virus. Step #2 Regrow Brain

Side Note: One of these days I'd like to be able to understand how Canadian research works so differently from U.S. and U.K. Don't ask me to prove this but
- University research seems to consistently punch above their weight (especially with patent-less collaborative contributions)
- nothing really strong and central like the CDC, NIH, etc (theoretically a negative) I guess because Health is strongly decentralized to Provinces
*** added link : *** it's relatively small and very new
- I see one provincial leader (Saskatchewan) alone pushing ahead immediate clinical studies of the Zamboni MS "Liberation" technique within their province (in response to patient demand)


Senior Member
this reminds me of that italian centenarian that puts the NGF in her eyes... she's still a senator...


Senior Member
this reminds me of that italian centenarian that puts the NGF in her eyes... she's still a senator...

Hi judderwocky,

Thanks for reminding me...yes an amazing woman... I remember reading about Rita Levi-Montalcini is her story

Is this the secret of eternal life?

Rita Levi-Montalcini won a Nobel Prize for discovering nerve growth factor. Now, at 100, she appears to be benefiting.

Most centenarians attribute their great age to some magic elixir or other. The longevity of the Italian scientist Rita Levi-Montalcini, who this week became the first Nobel Prize-winner to reach the age of 100, might be the result of a potion that is a little out of the ordinary: Professor Levi-Montalcini, it is said, puts her undiminished mental vigour down to regular doses of nerve growth factor (NGF) – the discovery that made her famous.

She was awarded the 1986 Nobel Prize for Medicine jointly with an American, Stanley Cohen, for her research into NGF: the proteins and amino-acids which enable the cells of the nervous system to grow and take on specialised tasks. Despite her age, Dr Levi-Montalcini, a neurologist and development biologist, still works every day at the European Brain Research Institute, which she founded in Rome.

During numerous celebrations this week, she claimed that her brain was more vigorous today than it was four decades ago. "If I'm not mistaken," she said, "I can say my mental capacity is greater than when I was 20 because it has been enriched by so many experiences, in the same way that my curiosity and desire to be close to those who suffer has not diminished."

According to Pietro Calissano, who collaborated with the professor on an article for Scientific American in which she announced her discovery in 1979, NGF may have played a direct role in her amazing vitality. "Every day, she takes NGF in the form of eye drops," he said, "but I can't say for sure if this is her secret. At the start, it seemed this molecule's effect was restricted to acting on the peripheral nervous system, but then it emerged that it has a very important role in the brain. Contrary to what was believed, the brain does not have a rigid structure but is in continuous movement, and NGF helps neurons – which we begin to lose between 10 and 15 years old – survive."