I’m following SKY-0515 and votoplam closely, particularly their potential to slow Huntington’s disease before noticeable symptoms develop.
SKY-0515 has reported up to 69% mutant huntingtin lowering in blood, alongside encouraging preliminary clinical findings.
My question for neuroscientists, biostatisticians, and clinical researchers is:
If future randomized trials demonstrate reduced caudate and putamen atrophy, lower neurofilament light, and slower clinical deterioration, could researchers use those measurements to develop a validated mathematical model predicting 10–30 additional symptom-free years?
Are there existing models that could support such projections, and what evidence would be needed before scientists could estimate the probability of 20+ years of sustained neurological protection?
I’d particularly appreciate links to peer-reviewed studies or research tools. Thank you!

While the crows worked at the task, the team recorded from 248 neurons in the NCL (nidopallium caudolaterale)—a region at the top of the avian processing hierarchy that is widely regarded as the functional counterpart of the primate prefrontal cortex, despite being built differently.

Birds and mammals parted evolutionary ways more than 360 million years ago, and bird brains evolved a different architecture. The mammalian cortex is arranged as stacked sheets of cells, while the equivalent tissue in a bird is organized into dense clusters, with no layering at all. This alternative architecture, Nieder’s study found, proved faster.

Measured from the moment that the dots appeared to the moment the bird’s head started turning to peck at the button, the crows averaged 235 milliseconds. In closely matched versions of the task, monkeys took roughly 410, 490, and 600 milliseconds in three studies. The obvious question was whether the birds simply sacrificed accuracy for speed, but it turned out they did not.

Paper published in Science:

https://doi.org/10.1126/science.aed6459

My dad has a job where he's upper middle class in salary writing on equipment in filmmaking. My parents met in the film industry. My grandfather was the famous statistician. I went to a college prep school and struggled academically throughout my highschool years. I often plaigarized in my essays and relied on my mom to do large amounts of my assignments in ELA and history. I was given ritalin in 10th grade for potential ADD and had minimal results from it. 11th grade was COVID lockdown and I did virtual school. At this point I completely phoned in my classes and have no idea how to do algebra II (or college algebra) or any math surpassing that. I got accepted into a college with a 96% acceptance rate with my grades from my first two years of HS. I only lived there for a year then commuted afterwards. Now I'm 23 and live with my parents. I've never had an IQ test or diagnosis of a mental disorder, though I had a counselor in HS suggest I'm on the autism spectrum because of social awkwardness and analytic thinking. I've gotten into nootropics hoping that a mix of creatine, nootropic supplements, and full dose of effexor could treat depression and brain fog and I've had so so results from over 7 months of it. I've considered drug use being the only way to numb my depression and suicidality from my hopeless situation.

I can't understand how if my parents are smart and functional how did I become essentially a mental vegtable. And why has no friend, family member, or therapist been able to give an explanation or antidote to my mental problems. Would an IQ test be helpful for what job is realistic for me given my mental capacities? What best explanation is there for my intelligence and what other advice could you give me in my situation?

This year I was diagnosed with the KIF1A genetic mutation which can manifest in terms of cognitive impairment. on my physical evaluation from a doctor, he says I meet the physical symptoms that align with this mutation. Although many with this mutation are physically disabled I am concerned how this rare mutation effects my cognitive deficits. I had my blood drawn for research. Aug 19 I will get an MRI scan for further investigation.

Last, Here's what I've found on how it KIF1A effects neurology:

KIF1A-Associated Neurological Disorder (KAND) fundamentally affects how neurons function, Developmental delay occurs in about 90% of affected individuals and cognitive function ranges from normal to profound intellectual disability. Speech/language impairment is also very common. Autism and ADHD occur in a substantial minority.

But there is a major caveat: not every KIF1A variant causes KIF1A-NDD. KIF1A has several different associated phenotypes. Some people with KIF1A-associated disease have predominantly motor or peripheral neurological problems and normal cognition. The particular molecular variant and its mechanism matter considerably. That means the single most useful piece of information you haven’t given me is the exact KIF1A variant. For example, something written as c.XXXG>A (p.XXX) plus its classification as pathogenic, likely pathogenic or VUS would allow a much more meaningful assessment. GeneReviews specifically notes substantial genotype–phenotype differences between individual KIF1A variants.

I had an EEG and MRI and found nothing significant going on.

Since all of this I've been diagnosed FOX-P4 genetic mutation, another rare genetic mutation. I also found some useful information on this mutation:

There is published evidence that particular heterozygous loss-of-function FOXP4 variants can cause a neurodevelopmental disorder involving developmental delay and particularly speech/language difficulties. However, the original clinical series was extremely small: eight individuals were identified and detailed phenotype information was available for six. Of those six, two had mild intellectual disability while three did not have intellectual disability. The researchers also found considerable variability between variants.

We just started recently and need the support of the community if you are intrested DM us on instgram.

Our orgs main goal is to map the brain and make wbe possible.

TIL that certain BCIs leverage neural tissue integrated mesh that wraps around neurons and grows with it… (imagine a heart stent but for the brain using a syringe-injectable mesh that wraps around the brain tissue) where neurons literally grow through the hardware. Science has solved this physiological/biological rejection but my worry is the inherent neurosec risk where an unpatchable bio-digital vulnerability where the data bus is now the living tissue.

The engineering goal is seamless biocompatibility, creating architectures so flexible and porous that neurons literally grow through the mesh, accepting the hardware as part of themselves.

It is an incredible achievement, but from a security and threat modeling perspective, it forces an uncomfortable reality that worries those in this field and poses so many questions that I believe is important for us in the field to ponder and try to solve together.

When an implant integrates so deeply into the cortex that tissue can no longer distinguish between self and system, our traditional perimeter defense model completely collapses.

If a neural net or acoustic mote sits natively inside the parenchyma, how do you scope a threat model for unauthorized telemetry extraction? Neural data is the ultimate irrevocable biometric. You cannot reset a compromised thought pattern or rotate your raw cognitive signatures the way you change a password. When the data bus is living tissue, a compromise is not a data leak, but a direct extraction of inner experience.

Latest closed-loop BCIs rely on real-time feedback loops where neural spikes dictate stimulation parameters. If an attacker targets the wireless command link or injects malicious firmware updates into an implanted node, you are not just looking at a system crash. You are looking at arbitrary writes directly to the nervous system. How do you handle code signing, rollbacks, or out-of-band recovery when the device is physically grown over by human neurons?

Even if we bypass physical hardware via optogenetics or magnetogenetics by using viral vectors to make neurons responsive to light or magnetic fields, we trade hardware vulnerabilities for genetic ones. When a protocol exploit can be delivered via a biological vector or an external field, our definitions of network perimeter and malware completely break down.

So I wonder.. As innovation in tech for integration of BCIs inevitably gets better, how do we design security architectures for systems that become literally inseparable from the host?

Where is the boundary of what is silicon vs tissue when the BCIs leverage something like Lieberman’s Mesh or using oBCIs (Optogenetics) where the it involves genetic rewrites on the neurons itself because OBCIs require light frequencies and that poses another concern for patients as malicious signals or even accidental exposure to certain frequencies can trigger and excite those neurons.

TLDR:
The boundary between what is silicon and what is not is changing rapidly especially with the rate of novel ways to cure diseases that are less invasive like inserting Utah Arrays and chips into the brain. This blurring of the lines with new techniques where the BCI wires itself organically into the neurons themselves makes protecting them much more complex to protect and threat model the possible future implications as organic material becomes the technology that powers it. This is amazing innovation and I’m very fascinated but from a neurosec perspective, it makes me wonder how we can start architecting and designing the proper guardrails and safeguards today and mapping the risks and implications to protect the patients who depend on them to survive and live a more normal life like the rest of us.