Proposed NJ bill could allow medical cannabis for sickle cell patients
TRENTON, N.J. (PIX11) — Anyone living with sickle cell anemia is a warrior, Leslie Davis-Primo will tell you.
'I've had three children, largely unassisted by medication -I didn't have any epidurals or whatever- and that's not to say that's a badge of honor, but I would gladly give birth to those three children back to back to back than to have a sickle cell crisis.'
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In the U.S., around 100,000 people have sickle cell, and it is most common among people of African descent.
A disorder affecting the shape of red blood cells, sickle cell patients endure excruciating pain.
Davis-Primo, of Somerset, has had it her whole life but didn't know until she had a crisis at age 23.
'The excruciating pain that you need oftentimes narcotic medication in the hospital or at home to take care of,' said Davis-Primo.
She is on a regiment of medications to treat her, but in New Jersey, there could one day be another approved option: medical cannabis. A bill in the State House would look to add the disease to the list of qualifying medical conditions.
'It's one of those diseases that is not recognized until we elevate it,' said Assemblywoman Verlina Reynolds-Jackson (D-NJ 15th District), the primary sponsor of the bill, which advanced through the Assembly Health Committee. 'It's under-researched, it's underfunded.'
Right now, in New Jersey, patients with conditions like cancer, ALS, PTSD, and many others are approved to use medical cannabis, but sickle cell is not yet on the list.
'Medical cannabis has been proven to help sickle cell anemia patients with this chronic pain that they have,' said Reynolds-Jackson. 'It's good for glaucoma, for other issues, it's even good for Crohn's disease, which I have.'
Should it be passed into law one day, Davis-Primo says she would consider taking advantage.
'That's the big thing for sickle cell nationwide and globally, really: access to care,' said Davis-Primo. 'This really, really makes me feel seen.'
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They force more TDP-43 to leave the nucleus and clump in the cytoplasm, causing further neurodegeneration that spreads to neighboring cells. This isn't the cause of all kinds of ALS, which is a complex disorder with many possible triggers. But in a 2019 study of postmortem brain samples, Dubnau and colleagues found that about one in five people with ALS had high levels of retrotransposon activation and TDP-43 dysfunction. Stay in the KnowSign up for the Knowable Magazine newsletter today As that ALS story was developing, other scientists were pursuing a connection between retrotransposons and another toxic protein in neurodegeneration: the tau protein, which twists into unruly tangles in the brain cells of people with Alzheimer's disease. It affects retrotransposons because it, like TDP-43, plays a role in keeping retrotransposons quiet, says Frost. That maintenance is a downstream effect of tau's association with the cell's interior skeleton. That skeleton is physically linked to the nucleus's skeletal structure, which in turn anchors the tightly wound-up DNA that silences retrotransposons. When tau goes bad, it changes the structure of the cell's main skeleton, making it more rigid. Frost and colleagues found that this structural defect propagates all the way to the nuclear skeleton and the chromosomes, just like tightening the strands on one side of a net could change the shape of the other side. This structural effect can unlock the tightly wound bits of chromosome in fruit flies, which damages their neurons, Frost reported in 2014. By 2018, she'd shown that tau problems unleashed jumping genes in the flies. 'They were legitimately jumping,' she says, going from their original chromosomal locations to other ones in the fly's brain cells. And the jumping genes contributed to the death of nerve cells. Frost and colleagues also studied mammals — mice — and in 2022 they reported that retrotransposons were also activated in mice with dysfunctional tau. Meanwhile, Frost and others examined brain cells from people who'd died of tau-related diseases such as Alzheimer's, which also revealed activated retrotransposons. 'They were legitimately jumping.' — BESS FROST This awakening of retrotransposons appears to happen early in the disease, according to the work of another team published in 2022. In blood samples from people on their way to developing Alzheimer's disease, the copying of retrotransposon genes into RNAs spiked, creating a 'retrotransposon storm,' just before their symptoms got bad enough to be labeled Alzheimer's. This growing body of evidence suggests that reactivating once-quiet retrotransposons, whether via dysfunctional tau or TDP-43, can create havoc. A potential treatment quickly comes to mind: Since these retrotransposons are a lot like viruses, scientists reason that antiviral drugs could help. Handily, doctors already have medications that stymie retroviruses: Millions of people take antiretroviral drugs to keep HIV in check or prevent it from gaining a foothold in their cells. Indeed, multiple studies over several years have investigated drugs from the HIV treatment playbook that block the enzyme reverse transcriptase. And in cells, flies and mice the drugs have dialed down retrotransposon activity and neurodegeneration. These medications are well understood and generally safe, and are already in trials for neurodegenerative disease. For example, researchers have tested the safety of a 24-week antiretroviral course in 40 people with ALS. Not only did most people safely complete the trial, but the levels of HERV-K in their blood went down, and they seemed to have a delay in progression of their ALS symptoms, the researchers reported in 2019. Frost recently published results from a small trial in which 12 people with early Alzheimer's disease took a reverse transcriptase inhibitor for 24 weeks. Her main goal was to determine if the treatment was safe, and it was — but the researchers also observed a drop in signs of inflammation in the participants' spinal fluid. Both Dubnau and Frost serve on the scientific advisory board for Transposon Therapeutics, which tested its own reverse transcriptase inhibitor in 42 people with ALS and/or FTD. The company says the drug was tolerable and yielded signs of less neurodegeneration and inflammation, plus a delay in the inevitable worsening of symptoms. The company is planning a larger trial; it also plans to test its drug in people with ALS, Alzheimer's and a related tau-based disease, progressive supranuclear palsy. Neither Frost nor Dubnau, who together recently summarized the field for the Annual Review of Neuroscience, believes that antiretroviral drugs alone are the solution to transposon-fueled Alzheimer's or ALS. As Douville notes, the drugs were designed to act only on specific target enzymes — they won't do anything to other retrotransposon genes, RNAs or proteins, which could also spur nerve-damaging inflammation. Meanwhile, scientists are looking beyond ALS and Alzheimer's as evidence accumulates that retrotransposons may contribute to other neurodegenerative and inflammatory conditions, such as Parkinson's disease and multiple sclerosis. 'It's really picking up speed,' Frost says. This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.
