T-Neuro Pharma takes a new approach to Alzheimer’s Disease diagnosis and treatment
ALBUQUERQUE — While the vast majority of Alzheimer’s Disease (AD) clinical trials have focused on decreasing beta-amyloid (the sticky protein fragment that gums up the brain and kills its cells) 99.6% of these trials have failed. The 0.4% that succeeded only treat symptoms, but do not stop progression of the disease.
T-Neuro Pharma’s technology is based on the breakthrough discovery of Dr. Christopher Wheeler out of Cedars-Sinai Medical Center in Los Angeles. Dr. Wheeler has demonstrated that beta-amyloid may only be a mere symptom of a deeper causative event- and he has discovered what that causative event is likely to be.
Dr. Wheeler has shown that one of the earliest events in Alzheimer’s disease (AD) progression is related to the immune system. He has shown that a type of abnormal aged immune cell is likely a major player in the earliest stages of Alzheimer’s disease. He has shown that these abnormal immune cells cause full AD symptoms in experimental animals ordinarily resistant to the disease. When these abnormal immune cells enter the brain, they cause the classic Alzheimer’s pathology, including Beta-Amyloid accumulation, neuro-inflammation and memory decline.
The immune cells responsible for this initial stage of AD are detectable in a human blood sample, and can identify an Alzheimer’s patient very early in the progression of the disease – as early as Mild Cognitive Impairment (MCI). Our data has shown that this simple blood test is more effective than costly MRI imaging, and invasive and painful Cerebral-Spinal Fluid sampling. T-Neuro is developing this discovery as a biomarker to detect early AD in both clinical trial and clinical laboratory settings.
In addition to the biomarker utility of this discovery, Dr. Wheeler has also shown that the T-cells can be blocked from entering the brain, preventing progression of AD. Ideally, the biomarker will be utilized to detect the disease early, then the treatment will be administered to prevent the disease from ever progressing.
This opens up opportunities for earlier, more beneficial intervention to patients than ever before. A reliable biomarker could streamline patient enrollment into future drug trials while allowing a simple, inexpensive, and non-invasive method to track their success. Looking forward, pharmacological elimination or inactivation of these peptide-specific T cells, either alone or combined with beta-amyloid-reducing drugs, promises to treat, prevent, and even cure AD in confirmed and at-risk patients with nominal side effects.