Alpha Cognition Inc. (Nasdaq: ACOG) (“Alpha Cognition” [ACI], or the “Company”), a biopharmaceutical company developing novel therapies for debilitating neurodegenerative disorders, today announced preclinical data supporting the continued development of ALPHA-1062 for the treatment of mild traumatic brain injury (mTBI). The data provides additional evidence of benefits of ALPHA-1062, in the treatment of mTBI resulting from repetitive blast trauma, a highly relevant military injury. Service related mTBI results in a high incidence of persistent physical and emotional challenges for patients, impacting their quality of life and that of their families. Additionally, a history of mTBI increases the risk of dementia diagnosis later in life.
Data analysis for this study, supported by the US Department of Defense and conducted in collaboration with US Department of Veterans Affairs investigators and the Seattle Institute of Biomedical and Clinical Research, has been concluded, demonstrating that ALPHA-1062 administration following blast induced mTBI, results in a notable reduction in indices of TBI associated neuropathology.
ALPHA-1062 administration reduced the brain levels of three toxic forms of a brain protein Tau. One of these forms (pTau 217) has been suggested to identify TBI patients at greater risk of long-term cognitive decline. It is also one of the earliest emerging biomarkers in Alzheimer’s disease. A second form of toxic Tau (pTau-S202/T205) can be found in very early-stage pathology in the brains of Alzheimer’s patients before the appearance plaques and tangles. The third form (pTau 231) is elevated in early Alzheimer’s disease and TBI. Taken together, reduction of these toxic forms of pTau suggests a potential role for ALPHA-1062 in the treatment of TBI and that this may additionally positively impact the risk of later developing Alzheimer’s disease.
Additional benefits of ALPHA-1062 were observed following blast trauma. High dose ALPHA-1062 reduced the numbers of myeloid cells which play a critical role in neuroinflammation and tissue repair, as well as the number of astrocytes, which regulate neurotransmitters like glutamate and GABA to support neuronal health. These changes are consistent with reduced neuroinflammation following ALPHA-1062 administration. Finally, nerve growth factor receptor expression, which plays an important role in neuronal survival, was increased in an ALPHA-1062 dose-dependent manner. “These outcomes are in agreement with those of an earlier pre-clinical study in a moderate TBI animal model, both studies demonstrated protective effects of ALPHA-1062, providing support for the continued development of ALPHA-1062 for the treatment of traumatic brain injury,” said Denis Kay, ACI’s Chief Scientific Officer.
Alpha Cognition’s next steps in this program will be to complete formulation of ALPHA-1062 for sublingual administration and conduct a bridging pharmacokinetic study vs. ZUNVEYL® (Benzgalantamine) and an existing intranasal formulation of ALPHA-1062.
