ALZHEIMER’S DISEASE
The ENDECE approach to treating Alzheimer’s Disease patients targets two additional core pathologies; chronic inflammation and demyelination of the brain tissue.
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 their mid 60’s.
Beta-amyloid plaques and tau-tangles in the brain have been considered the main causes of Alzheimer’s Disease (AD). However, neither the burden of beta-amyloid plaques nor their removal correlate with cognitive performance in Alzheimer’s Disease patients.
ALZHEIMER’S DISEASE CORE PATHOLOGIES
Accumulating evidence suggests that chronic inflammation (neuroinflammation) may not only be an important additional cause of Alzheimer’s Disease (AD), but may be a central mechanism driving Alzheimer’s Disease progression.
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.
“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
ENDECE APPROACH TO ALZHEIMER’S DISEASE
NDC-1308
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)