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Pioneering Science


Intracellular Magnesium in Synaptic Terminal:
Critical Regulator of Synaptic Density and Plasticity

Neurocentria discovered-
Elevation of intracellular magnesium is critical for prevention of synapse loss via:

Improvement of mitochondria function and elevation of
ATP production

Prevention and attenuation of neuroinflammation via 
normalization of
NF-kB signaling

Reduction of probability of 
neurotransmitter release, venting synaptic hyperexcitability

Reduction of Amyloid β deposition

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•Small molecule: L-Threonate Magnesium Salt (L-TAMS, NRCT-101)

•Elevates Mg2+ and L-Threonate in the CSF

•Only known compound that effectively increases Mg2+ in the synaptic terminal

•Increases synaptic density and plasticity

•Improves cognition and emotional regulation

Pioneering Clinical Programs


The Burden:

• ~17 million people in the US have ADHD

• Only 10% are treated

• Heavy burden on patients and families;

ADHD affects performance and mood, and causes

difficulties in workplace environments and

challenges with family life

 Current treatments:

• Do not improve quality of life and executive function

• Stimulants – impose significant side-effects

Non-stimulants – insufficient efficacy

• Act on monoaminergic synapses, a target developed

decades ago

Neurocentria's Path Forward:


• Pathophysiology of ADHD involves dysfunction of

glutamatergic synapses in the prefrontal cortex (PFC)

• NRCT-101SR improves glutamatergic synapse function in

PFC to address ADHD (novel drug class)


No novel treatments are under investigation



The Burden:

• 13% of adults in the US (34M) are treated

with antidepressants

• Heavy burden on patients and their families: persistent

sadness, loss of interest, difficulties with sleep, decreased

energy level, cognitive impairment and suicidal thoughts

• Cause: currently, the leading hypothesis is that imbalance

of monoamines such as serotonin is the cause for

depression, hence SSRIs are massively prescribed.

This hypothesis has been recently questioned.

Neurocentria's Path Forward:

• Recent studies suggest that the pathophysiology of

MDD involves synapse loss in the prefrontal cortex (PFC).

Our research suggests that the synapse loss during

depression is caused by reduction of

intracellular magnesium.

• The API of NRCT-101SR is an endogenous molecule,

naturally present in the brain and regulates

magnesium in synapses

• NRCT-101SR increases glutamatergic synapse density and

improves synaptic plasticity in the PFC to normalize

emotional regulation and address cognitive dysfunction

(novel drug class)

Alzheimer's Disease

The Burden:

• ~30 million people worldwide and ~6 million in the US

suffer from AD, expected to double by 2050

• Heavy burden on patients, families, care givers and the

health system

• No cure available; the established drugs address

symptoms only

• Recently approved drugs aiming to treat the pathology

have only modest effects and bear risk for

serious side-effects

• High failure rate of AD drug development suggests that

AD may not be treatable at advanced stages

Neurocentria's Path Forward:

• Synapse loss is hallmark of AD; NRCT-101SR

prevents synapse loss

• Clinical data shows NRCT-101SR improves cognition

and mood in older adults and those with early AD

• Best therapeutic approach is prevention or early treatment;

NRCT-101SR has shown an excellent safety profile,

making it a good candidate for preventional treatment


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