Regarding the Cornell study for Alzheimer’s Disease and hinting at the neuro-inflammatory underpinnings of the disease I found this just published case report of a woman given psilocybin who regained, at least for a time, significant functional and cognitive capacity in the face of a 10 year decline with AD quite fascinating:
https://www.frontiersin.org/journals/neurosci...13281/full
“Approximately 19 h post-administration, spontaneous autobiographical speech emerged. Over subsequent days and weeks, functional improvements included restoration of urinary continence, improved ambulation, autonomous dressing, increased emotional responsiveness, sustained social interaction, contextual memory retrieval, preserved working memory for social context, and spontaneous conversational engagement.”
From your posted linked article:
https://www.clinicaltrialvanguard.com/news/cy...s-disease/
“What the trial lacks in size it attempts to compensate for with imaging precision: the primary endpoint measures changes in brain inflammation and microglial activation using advanced PET imaging, the same kind of quantitative tool that has been used to distinguish patients with early Alzheimer’s from healthy controls in prior translational work.
The rationale centers on CCR5, a chemokine receptor that leronlimab blocks by binding directly to the receptor on immune cells. Preclinical evidence links CCR5 to synaptic plasticity, microglial signaling, and blood-brain barrier stability.”
https://pmc.ncbi.nlm.nih.gov/articles/PMC11547910/
Psilocin, the Psychoactive Metabolite of Psilocybin, Modulates Select Neuroimmune Functions of Microglial Cells in a 5-HT2 Receptor-Dependent Manner
“While the aggregation of amyloid β and the hyperphosphorylation of tau play well-established roles in the pathophysiology of Alzheimer’s disease (AD), the involvement of persistent neuroinflammation in the development and progression of this and other neurodegenerative disorders is increasingly accepted [1]. Neuronal death and neuroinflammatory responses in AD are accompanied by the chronic overactivation of glial cells, particularly microglia [2,3]. When confronted with abnormal protein aggregates, microglia facilitate the innate neuroimmune response. In part, this involves the clearance of harmful particles by phagocytosis and the release of cytokines, such as the pro-inflammatory tumor necrosis factor (TNF), and cytotoxins, including reactive oxygen species (ROS) and nitric oxide (NO) [4]. While these functions are essential for mounting an effective acute immune response, neurodegeneration, once triggered, leads to the chronic adverse reactivity of microglia. This causes the sustained secretion of pro-inflammatory mediators and excess phagoptosis, contributing to neuronal death [5,6]; therefore, anti-inflammatory therapies aimed at ameliorating reactive microglia represent feasible options in the search for effective treatments for these disorders”
https://www.frontiersin.org/journals/neurosci...13281/full
“Approximately 19 h post-administration, spontaneous autobiographical speech emerged. Over subsequent days and weeks, functional improvements included restoration of urinary continence, improved ambulation, autonomous dressing, increased emotional responsiveness, sustained social interaction, contextual memory retrieval, preserved working memory for social context, and spontaneous conversational engagement.”
From your posted linked article:
https://www.clinicaltrialvanguard.com/news/cy...s-disease/
“What the trial lacks in size it attempts to compensate for with imaging precision: the primary endpoint measures changes in brain inflammation and microglial activation using advanced PET imaging, the same kind of quantitative tool that has been used to distinguish patients with early Alzheimer’s from healthy controls in prior translational work.
The rationale centers on CCR5, a chemokine receptor that leronlimab blocks by binding directly to the receptor on immune cells. Preclinical evidence links CCR5 to synaptic plasticity, microglial signaling, and blood-brain barrier stability.”
https://pmc.ncbi.nlm.nih.gov/articles/PMC11547910/
Psilocin, the Psychoactive Metabolite of Psilocybin, Modulates Select Neuroimmune Functions of Microglial Cells in a 5-HT2 Receptor-Dependent Manner
“While the aggregation of amyloid β and the hyperphosphorylation of tau play well-established roles in the pathophysiology of Alzheimer’s disease (AD), the involvement of persistent neuroinflammation in the development and progression of this and other neurodegenerative disorders is increasingly accepted [1]. Neuronal death and neuroinflammatory responses in AD are accompanied by the chronic overactivation of glial cells, particularly microglia [2,3]. When confronted with abnormal protein aggregates, microglia facilitate the innate neuroimmune response. In part, this involves the clearance of harmful particles by phagocytosis and the release of cytokines, such as the pro-inflammatory tumor necrosis factor (TNF), and cytotoxins, including reactive oxygen species (ROS) and nitric oxide (NO) [4]. While these functions are essential for mounting an effective acute immune response, neurodegeneration, once triggered, leads to the chronic adverse reactivity of microglia. This causes the sustained secretion of pro-inflammatory mediators and excess phagoptosis, contributing to neuronal death [5,6]; therefore, anti-inflammatory therapies aimed at ameliorating reactive microglia represent feasible options in the search for effective treatments for these disorders”
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