That's super unusual, as clemastine is another first generation antihistamine that's also anticholinergic. Other anticholinergic antihistamines have been shown to lead to increased dementia effects in users.
Pretty interesting. There was a study about Clemastine use as a potential treatment/prolonging for ALS, but it did not show any significant benefit at preventing/delaying neuron death. I bring it up ALS because there are certain treatments for MS (like IVIG Infusions) that can also be beneficial for ALS patients.
Clemastine fumarate is an old school antihistamine!
Original title: "Clemastine fumarate promotes myelin repair in a nonhuman primate model of demyelination characterized by absent spontaneous remyelination"
"Abstract. Promotion of remyelination has become a new therapeutic avenue, to prevent neuronal degeneration and promote recovery in white matter diseases such as multiple sclerosis. Clemastine fumarate among several promyelinating agents, has been validated as a promyelinating agent in rodents and has led to a first successful double-blind, placebo-controlled clinical trial evaluating a remyelinating therapy for multiple sclerosis (MS) [A. J. Green et al., Lancet 390, 2481–2489 (2017)]. To date, most of promyelinating strategies have been developed in short-lived rodent models of demyelination, which spontaneously repair. Well-defined nonhuman primate models closer to man would allow to efficiently advance therapeutic approaches, and namely to assess noninvasively, their efficacy in promoting functional repair. We developed a nonhuman primate model of optic nerve demyelination which leads to failed remyelination, progressive neuronal degeneration, and visual dysfunction, thus recapitulating several features of MS lesions and providing the missing link to translate emerging preclinical therapies to the clinic for myelin disorders such as multiple sclerosis [N. Sarrazin et al., Proc. Natl. Acad. Sci. U.S.A. 119, e2115973119 (2022)]. We used this model to assay the therapeutic benefits of clemastine. Our histological and ultrastructural findings show that clemastine is able to overcome the failed remyelination of the nonhuman primate optic nerve. We also used visual evoked potential, optical coherence tomography, and electroretinogram as noninvasive means to follow up the optic nerve de/remyelination process and correlated these findings with postmortem analysis to establish the safety and efficacy of clemastine therapy in promoting functional and morphological recovery in nonhuman primates. We demonstrate that clemastine can overcome chronic demyelination in nonhuman primates."
That's super unusual, as clemastine is another first generation antihistamine that's also anticholinergic. Other anticholinergic antihistamines have been shown to lead to increased dementia effects in users.
https://en.wikipedia.org/wiki/H1_antagonist
Pretty interesting. There was a study about Clemastine use as a potential treatment/prolonging for ALS, but it did not show any significant benefit at preventing/delaying neuron death. I bring it up ALS because there are certain treatments for MS (like IVIG Infusions) that can also be beneficial for ALS patients.
https://pmc.ncbi.nlm.nih.gov/articles/PMC10568021/
Clemastine fumarate is an old school antihistamine!
Original title: "Clemastine fumarate promotes myelin repair in a nonhuman primate model of demyelination characterized by absent spontaneous remyelination"
"Abstract. Promotion of remyelination has become a new therapeutic avenue, to prevent neuronal degeneration and promote recovery in white matter diseases such as multiple sclerosis. Clemastine fumarate among several promyelinating agents, has been validated as a promyelinating agent in rodents and has led to a first successful double-blind, placebo-controlled clinical trial evaluating a remyelinating therapy for multiple sclerosis (MS) [A. J. Green et al., Lancet 390, 2481–2489 (2017)]. To date, most of promyelinating strategies have been developed in short-lived rodent models of demyelination, which spontaneously repair. Well-defined nonhuman primate models closer to man would allow to efficiently advance therapeutic approaches, and namely to assess noninvasively, their efficacy in promoting functional repair. We developed a nonhuman primate model of optic nerve demyelination which leads to failed remyelination, progressive neuronal degeneration, and visual dysfunction, thus recapitulating several features of MS lesions and providing the missing link to translate emerging preclinical therapies to the clinic for myelin disorders such as multiple sclerosis [N. Sarrazin et al., Proc. Natl. Acad. Sci. U.S.A. 119, e2115973119 (2022)]. We used this model to assay the therapeutic benefits of clemastine. Our histological and ultrastructural findings show that clemastine is able to overcome the failed remyelination of the nonhuman primate optic nerve. We also used visual evoked potential, optical coherence tomography, and electroretinogram as noninvasive means to follow up the optic nerve de/remyelination process and correlated these findings with postmortem analysis to establish the safety and efficacy of clemastine therapy in promoting functional and morphological recovery in nonhuman primates. We demonstrate that clemastine can overcome chronic demyelination in nonhuman primates."