{"id":33895,"date":"2023-09-10T22:36:16","date_gmt":"2023-09-10T22:36:16","guid":{"rendered":"https:\/\/danielsmarketingblc.com\/CuratedProducts\/?p=33895"},"modified":"2023-09-10T22:36:16","modified_gmt":"2023-09-10T22:36:16","slug":"study-evaluating-intranasal-anti-cd3-for-treatment-of-alzheimers-disease-published-within-the-pnas-journal","status":"publish","type":"post","link":"https:\/\/danielsmarketingblc.com\/CuratedProducts\/2023\/09\/10\/study-evaluating-intranasal-anti-cd3-for-treatment-of-alzheimers-disease-published-within-the-pnas-journal\/","title":{"rendered":"Study evaluating intranasal anti-CD3 for treatment of Alzheimer\u2019s disease published within the PNAS journal"},"content":{"rendered":"
\n <\/span><\/p>\n

Tiziana Life Sciences Ltd. (\u201cTiziana\u201d or the \u201cCompany\u201d), a biotechnology company developing breakthrough immunomodulation therapies via novel routes of drug delivery, today announced acceptance of a publication, \u201cNasal Administration of anti-CD3 monoclonal antibody (mAb) ameliorates disease in a mouse model of Alzheimer\u2019s disease\u201d, within the preeminent\u00a0journal, Proceedings of the National Academy of Sciences<\/em> (PNAS), that supports foralumab\u2019s mechanism as a possible treatment for Alzheimer\u2019s disease (AD), a difficult-to-treat neuroinflammatory disease. That is the second publication pertaining to intranasal administration of anti-CD3 monoclonal antibody this yr to be published in PNAS.<\/p>\n

This study shows that intranasal anti-CD3 ameliorates disease in a rodent model of AD by targeting microglial activation within the brain and brain gene expression independent of affecting amyloid beta deposition. These studies discover a novel approach to treat Alzheimer’s disease.<\/p>\n

Howard L. Weiner, M.D., a Robert L. Kroc Professor of Neurology on the\u00a0Harvard Medical School, Director and Founding father of the Partners Multiple Sclerosis Center and Co-Director of the\u00a0Center for Neurologic Diseases\u00a0at Brigham and Women\u2019s Hospital, a founding member of\u00a0Mass General Brigham Healthcare System and Chairman of Tiziana’s\u00a0Scientific Advisory Board, stated, \u201cI’m proud to be the senior writer on this seminal publication showing that anti-CD3 mAb mitigates Alzheimer\u2019s disease in a rodent model. Remarkably, we found this profit occurred independent of reduction of amyloid beta plaque within the brain. This finding demonstrates a singular mechanism of motion that may now be tested in humans using foralumab, a totally human anti-CD3 mAb, foralumab, wherein we modulate microglia by inducing T cells<\/a> within the periphery that migrate to the brain. This represents a singular approach to treating Alzheimer\u2019s disease that would also potentially be employed together with anti-amyloid therapy. The neuromodulation of the T cell inflammatory response we observed within the brains of Alzheimer\u2019s mice is consistent with multiple sclerosis research we’ve got conducted on the Ann Romney Center and validates our scientific rationale for testing foralumab in Alzheimer\u2019s patients after the recent IND clearance by the USA Food and Drug Administration.\u201d<\/p>\n

\n

We\u2019ve now have had two seminal publications within the esteemed journal PNAS<\/em> related to novel and significant research on intranasal anti-CD3. It has been established through each publications that intranasal anti-CD3 positively modulates the immune system allowing Tiziana to explore foralumab in multiple neuro-inflammatory disease indications along with our ongoing research in non-active secondary progressive multiple sclerosis. We consider this scientific publication, together with the groundbreaking research constantly being conducted by our partners at Brigham and Women\u2019s Hospital led by Dr. Weiner, greatly increases the utilization potential of our foralumab portfolio.\u201d<\/p>\n

Gabriele Cerrone, Executive Chairman, Founder and Acting Chief Executive Officer, Tiziana<\/p>\n<\/blockquote>\n

Study rationale<\/h2>\n

Alzheimer’s disease is a neurodegenerative disease characterised by amyloid beta (A\u03b2) plaques, neurofibrillary tangles, and microglial activation. Neuroinflammation is a significant component of AD. Microglia are the first immune cells of the brain that help each maintain homeostasis and react to injury. Studies showing activated microglia and astrocytes surrounding A\u03b2 plaques suggest significant involvement of inflammatory pathways in Alzheimer\u2019s disease. Therapies targeting A\u03b2 have shown positive effects in subjects with AD. Nasal anti-CD3 has been shown to treat animals with a progressive type of experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, by inducing regulatory T cells that dampen microglial inflammation within the brain.<\/p>\n

<\/p>\n

Study design<\/h2>\n

On this study, mice were treated 3 times per week with intranasal anti-CD3 for five months and compared against isotype control or saline. Within the treated mice, the study found modulation of the activated microglia phenotype, changes in gene expression patterns within the brain and improved cognition, which all occurred independent of affecting amyloid beta deposition. Modulation of activated microglia was measured in treated mice by sorting the microglia using microglia-specific markers and performing a gene expression evaluation using the Nanostring mouse myeloid panel and comparing treated mice versus control. Changes in gene expression were measured within the cortex and hippocampus. Cognition was measured including spatial learning and long- and short-term memories as assessed by the Morris water maze and the novel arm Y-maze behavioral test. Amyloid beta accumulation was measured by immunofluorescence within the hippocampus and prefrontal cortex areas of the brain.<\/p>\n

\n

Source:<\/p>\n

Journal reference:<\/p>\n

\n

Lopes, J. R., et al<\/em>. (2023) Nasal administration of anti-CD3 monoclonal antibody ameliorates disease in a mouse model of Alzheimer\u2019s disease. PNAS<\/em>. doi.org\/10.1073\/pnas.2309221120<\/a>.<\/p>\n<\/div>\n<\/div><\/div>\n","protected":false},"excerpt":{"rendered":"

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