In October 2021, Silo Pharma (OTCQB: SILO) entered
into a sponsored research agreement (“SRA”) with Columbia University to investigate and advance psychedelic therapeutics for Alzheimer’s Disease (“AD”).
SRA’s grant Silo access to world-class research facilities to sponsor potential life-changing research while offering Silo licensing opportunities for groundbreaking psychedelic remedies.
Columbia University Irving Medical Center (“CUIMC
”), an “internationally recognized leader” in research and therapeutic development, partnered with Silo to study psychedelics’ ability to improve, slow, or even reverse functional decline and memory loss associated with Alzheimer’s disease.
Associate Professor of Clinical Neurobiology, Dr. Christine Ann Denny
, helming the research for Silo, explores “the molecular mechanisms underlying learning and memory,” and has co-authored research detailing psychedelic treatment for depression, mechanisms of age-related memory loss, mood improvement and stress reduction.
Silo Parma CEO Eric Weisblum expressed encouragement on partnering with Dr. Denny and Columbia University. “To be able to bring hope and possibly a therapeutic to patients suffering from Alzheimer’s disease is an exciting proposition for Silo Pharma.”
The Mayo Clinic defines Alzheimer’s Disease
as an incurable and progressive “neurologic disorder that causes the brain to shrink (atrophy) and brain cells to die. [AD] is the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that affects a person’s ability to function independently.”
The National Institute on Aging
(“NIA”), one of the 27 institutes and centers forming The National Institutes of Health (“NIH”), offers the following AD facts:
- Over 6 million Americans, mostly over 65, may have AD-related dementia.
- AD ranks seventh among all leading causes of US deaths and is the most “common cause of dementia among older adults.”
- Early-onset AD affects people between their 30s and mid-60s though represents under 10% of Alzheimer’s patients.
- Behavioral symptoms include sleeplessness, wandering, agitation, anxiety, and aggression.
- Diagnosis includes performing standard medical tests and various brain scans, ascertaining medical history, personality or behavioral changes, current mental health issues and cognitive, memory and self-care abilities.
- AD is degenerative and worsens at different rates among patients, from early mild AD symptoms to complete dependence on caretakers.
- Alzheimer’s Disease International states that the “annual global cost of dementia is now above US$ 1.3 trillion and is expected to rise to US$ 2.8 trillion by 2030.”
Currently, there is no AD cure. Studies have pointed towards preventative methods, according to the AAFP
, “that may affect the incidence of [AD], such as the use of dietary supplements and pharmacologic agents” as well as lifestyle choices and circumstances, including “diet, socioeconomic factors, medical conditions, and environmental exposures,” though these studies have been unable to prove actual causation or efficacy.
Drugs used to treat
mild to severe AD symptoms include “galantamine, rivastigmine, and donepezil … cholinesterase inhibitors that … may help reduce or control some cognitive and behavioral symptoms.” Science can’t explain why these drugs work and all lose efficacy over time as AD progresses. Side effects include “nausea, vomiting, diarrhea, decreased appetite, dizziness, headache.”
, the only FDA-approved disease-modifying drug for AD treatment, targets “brain lesions associated with Alzheimer’s,” though effectiveness has only been studied on those with early or mild symptoms. Aducanumab is “administered intravenously (“IV”) via a 45- to 60-minute infusion every 4 weeks” and may “slow the progression
of the earliest symptoms…” Side effects can be serious, including “brain inflammation called amyloid-related imaging abnormalities (‘ARIA’), which involves brain bleeding, brain swelling, or a combination of the two.”
A peer-reviewed article in Frontiers in Synaptic Neuroscience
illustrates the interest in psychedelics by the AD medical community, particularly “their potential to stimulate neurogenesis [process of generating functional neurons
], provoke neuroplastic changes [structural and functional changes to the brain
] and reduce neuroinflammation. This inevitably makes them interesting candidates for therapeutics in dementia.” Some important points raised in the article:
Adverse effects of psychedelics: From anecdotes and misinformation to systematic science
- Psychedelics induce brain plasticity and modify connectivity between brain regions and there is considerable anecdotal evidence of cognitive benefits from micro-dosing—a dose that does not cause perceptual change or impair functioning…
- A 2018 uncontrolled, open-label naturalistic trial found increased cognitive fluency, flexibility, and originality amongst the 33 participants at various micro-doses of psilocybin… In general, the medication was well tolerated with no serious adverse events or drop-outs.
- In treatment-resistant depression, 10 mg and 25 mg of psilocybin given 1 week apart … led to clinical response or remission in 14 participants sustained at assessment 5 weeks later. This effect persisted at 6 months follow up despite no further treatment…
- In AD there is a reduction in global brain glucose metabolism … In the only psilocybin FDG-PET study to date … ingestion of a 15 mg or 20 mg dose increased global brain glucose metabolism by approximately 25% …
- All known genetic and environmental risk factors for AD are associated with increased inflammation … Psychedelics have been shown to have potent anti-inflammatory properties and … may represent a unique anti-inflammatory overwhelmingly targeted to brain tissue …
, in the Journal of Psychopharmacology
states that “The first RCT [randomized controlled trial] comparing psilocybin to a conventional selective serotonin reuptake inhibitor (‘SSRI’) antidepressant found the former to be as efficient at reducing symptoms of depression, and with fewer side effects … Most researchers now consider classic psychedelics to be non-toxic, that is, they do not damage mammalian organ systems, and as physiologically safe, even in very high doses…”
Alongside Silo’s work with Columbia University, they’re also exploring methods for delivering psychedelic therapeutics in extremely targeted doses. Partnering with the University of Maryland Baltimore, Silo believes central nervous system (“CNS”) homing peptides
can deliver a microdose “payload” to inflamed tissue while bypassing healthy organs. A Silo Pharma news release says, “the ability to deliver psilocybin and other psychedelic compounds directly to targeted areas of the body … could be significant by increasing the efficacy of the treatment while reducing the amount of medicine needed.”
Silo’s partnership developing Zylo Therapeutics Z-pod technology for sustained transdermal delivery
delivers time-released ketamine or psilocybin which will, says Silo CEO Eric Weisblum, “allow [Silo] to explore both the safety and efficacy of our therapeutics while hopefully diminishing the hallucinogenic effects of psychedelics. We believe that Zylo’s patented technology will allow us to reach potential patients suffering from dysphagia, an inability to swallow affecting those with severe AD.
Silo is committed to serving patients, families and caregivers worldwide struggling with Alzheimer’s Disease. We eagerly await results from recent research which utilizes cutting-edge psychedelic therapeutics and traditional treatments.”
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