Beta-amyloid plaques and tau-tangles in the brain are considered the main causes of Alzheimer’s Disease (AD). To date, Alzheimer’s Disease has been an irreversible and progressive brain disorder that reduces memory, cognition, and one’s ability to execute the simplest tasks. Symptoms usually appear when a patient is in mid 60’s.


Current treatments may help manage Alzheimer’s Disease symptoms in some people. However, there is no cure for this devastating disease.

Accumulating evidence suggests that chronic inflammation (neuroinflammation) may not only be an important additional cause of AD, but may be a central mechanism driving Alzheimer’s Disease progression.

“It’s the inflammation that occurs in response to plaques and tau-tangles (neuroinflammation), that is the primary killer of neurons, which leads to cognitive deficits.”

Dr. Rudolph Tanzi
Director, Genetics and Aging Research Unit
Mass General Hospital

Memory decline in Alzheimer’s patients may be related to demyelination in the prefrontal and superior temporal regions of the left hemisphere (hippocampus) of the brain.

Since myelination of axons is a prerequisite for the higher functions within the CNS, regeneration of functional myelin (remyelination) particularly within the hippocampus, might be conducive to improvements in cognition in AD patients.



NDC-1308 has a dual mechanism of action that may reduce inflammation and induce remyelination in neurodegenerative diseases such as Alzheimer’s Disease, which could effectively reverse the damage.

NDC-1308 is a small molecule targeting the additional core pathologies that may characterize Alzheimer’s Disease (AD).


Anti-inflammation: NDC-1308 directly targets and upregulates the LPL gene within macrophages; the active LPL protein polarizes the macrophages from the M1 state (pro-inflammatory) to the M2 state (anti-inflammatory)


Remyelination: NDC-1308 directly targets and upregulates key genes within oligodendrocyte progenitor cells (OPCs); the active proteins then induce the OPCs to differentiate into mature, myelinating oligodendrocytes that remyelinate demyelinated axons (including the hippocampus)