Alzheimer’s disease (AD) is biologically defined by the accumulation of β-amyloid (Aβ) plaques and phosphorylated tau (P-tau) tangles, which appear decades before cognitive symptoms (Jack et al., 2018). Early detection and targeted intervention remain limited by the lack of scalable, non-invasive diagnostics and by the difficulty of delivering therapeutics across the blood–brain barrier (BBB) (Gao et al., 2025; Kwak et al., 2024; Meairs, 2015). This paper proposes the Quantum-CRISPR Epigenome-Targeted Theranostic System (Q-CETS), a platform integrating quantum nanodiamond biomarker sensing with MRI-guided, Focused Ultrasound (FUS) delivery of dCas9-based epigenome-modifying tools. Q-CETS aims to identify individuals in the earliest stages of the Alzheimer’s continuum and intervene directly in the molecular drivers of pathology. By combining non-invasive early detection and precise gene-regulatory modulation, Q-CETS establishes a comprehensive, biologically targeted framework for preventing AD before neurodegeneration begins.
Quantum-CRISPR Epigenome-Targeted Theranostic System (Q-CETS): A Next-Generation Platform for Alzheimer’s Prevention and Diagnosis
Abstract
I. What Would It Measure?
The Q-CETS diagnostic module would measure the earliest molecular signals of Alzheimer’s disease: soluble Aβ oligomers and P-tau species circulating in peripheral biofluids. These biomarkers are the foundation of the AT(N) classification framework and precede clinical symptoms by up to twenty years, making them ideal targets for population-level, presymptomatic screening (Jack et al., 2018). Q-CETS employs Quantum Sensing Nanodiamonds (QSNPs) containing nitrogen-vacancy (NV) centers, which detect nanoscale magnetic and electric field perturbations generated when functionalized antibodies bind Aβ or P-tau. Binding events modulate NV fluorescence lifetimes, creating a quantifiable optical signal that corresponds to biomarker concentration (Tan et al., 2022; Chaparro et al., 2023; Barry et al., 2020). This enables a novel, quantum-level molecular measurement in peripheral fluids such as blood or saliva—an approach fundamentally different from PET imaging or CSF sampling. Because NV-center fluorescence responds on microsecond timescales and is highly sensitive to small biomolecular interactions, the system could deliver instantaneous biomarker readouts during routine clinical workflows (National Institute on Aging, 2024). Q-CETS therefore fills a critical gap by providing sensitive, non-invasive, scalable early detection grounded in the physical behavior of quantum spin states.
II. What Would the Equipment Look Like?
Q-CETS consists of two linked technologies: a diagnostic device for early identification and a therapeutic delivery system for targeted intervention. The diagnostic device, the Quantum Early Test (QET-Scanner), is a compact benchtop instrument operating through low-power laser excitation and high-precision photodetection of NV fluorescence. It contains microfluidic channels for sample handling and a processing unit running machine-learning models that classify Aβ and P-tau levels. With a size comparable to a standard blood analyzer and weighing under 20 pounds, the QET-Scanner could be deployed in primary-care clinics, community centers, or pharmacies for rapid screening (Tan et al., 2022; Zhang et al., 2024). The therapeutic system is used only when Q-CETS indicates elevated risk. It consists of a biodegradable polymeric nanocarrier made from poly(β-amino ester) (PBAE) coated with polyethylene glycol to improve circulation time and reduce immune activation (Kwak et al., 2024). The nanoparticle includes embedded SPIONs, which allow MRI visualization and magnetic steering (Chakraborty et al., 2023). It carries mRNA encoding a catalytically inactive Cas9 (dCas9) fused to epigenetic effector domains and paired with sgRNAs targeting AD-related genes such as APP, PSEN1, and MAPT. Delivery is guided by MRI and assisted by Focused Ultrasound, which temporarily opens the BBB through microbubble-assisted acoustic cavitation, permitting nanoparticles to reach deep brain targets safely (Meairs, 2015). The two devices rely on distinct physical principles—quantum coherence, optical fluorescence, magnetic resonance, and ultrasound propagation—yet together form a unified theranostic platform capable of both identifying and modulating the earliest stages of AD biology.
III. What Would the Data Look Like?
The diagnostic module generates optical emission data from NV-center fluorescence signals that shift based on molecular binding events. These measurements occur on microsecond timescales and require minimal computational processing aside from spectral deconvolution and machine-learning-based biomarker quantification (Tan et al., 2022). Output data include concentrations of Aβ and P-tau reported in pg/mL, along with automated AT-framework classification (Jack et al., 2018). Because measurements are performed on small fluid samples, data storage requirements are modest and allow near-instantaneous reporting. The therapeutic component generates MRI data representing the distribution and accumulation of SPION-labeled nanocarriers in targeted brain regions. T2*-weighted MRI sequences provide sub-millimeter spatial resolution, visualizing how nanoparticles travel through opened BBB regions and confirming their successful localization to hippocampal or cortical areas implicated in early AD (Chakraborty et al., 2023). Additional imaging overlays can display predicted dCas9 editing activity, integrating pre-intervention biomarker levels from the diagnostic module with post-intervention imaging. Data volumes range from megabytes to gigabytes depending on MRI duration, but standard clinical reconstruction methods and machine-learning-based prediction models streamline real-time interpretation (Meairs, 2015).
IV. What Are the Limitations and Challenges?
Despite its potential, Q-CETS faces significant biological, physical, and regulatory challenges. FUS must be carefully calibrated to ensure safe BBB opening without damaging vascular or neuronal tissue, and nanoparticle size must remain under approximately 100 nm to cross the BBB effectively, limiting payload capacity (Kwak et al., 2024; Meairs, 2015). NV-center quantum sensors are highly sensitive but susceptible to environmental noise and decoherence, requiring shielding and advanced signal-processing techniques to maintain accuracy (Barry et al., 2020; Zhang et al., 2024). Engineering challenges include producing nanocarriers with consistent size, charge, and magnetic properties at scale, ensuring long-term biocompatibility, and avoiding oxidative stress or immune responses associated with SPIONs or nanodiamond surfaces (Chakraborty et al., 2023). The integration of quantum diagnostics with gene-regulatory therapeutics also presents unprecedented regulatory complexity, as both fields are subject to strict translational and ethical standards. Biologically, dCas9-based epigenome editing must achieve stable yet reversible modulation of target gene expression while minimizing off-target effects. Delivering CRISPR machinery to long-lived neurons introduces uncertainties about duration of action and long-term safety (Kwak et al., 2024). Ethical concerns must also be addressed, particularly when intervening in asymptomatic individuals identified solely by molecular risk markers (Jack et al., 2018).
V. What Would This Enable?
If fully realized, Q-CETS would redefine both Alzheimer’s research and clinical practice. The QET-Scanner could deliver population-wide presymptomatic screening, identifying at-risk individuals in routine healthcare settings without radiation or invasive sampling (Jack et al., 2018). Personalized nanocarriers could then deliver epigenetic interventions tailored to each patient’s molecular and genetic risk profile, providing a precision-medicine approach capable of modulating Aβ and tau pathways before irreversible neurodegeneration occurs (Kwak et al., 2024). In research settings, Q-CETS would allow for longitudinal monitoring of disease-related biomarkers in combination with direct visualization of therapeutic effects, offering insights into early pathophysiology that remain beyond the reach of current imaging technologies. The platform could also be adapted to other neurodegenerative conditions characterized by protein aggregation or dysregulated gene expression, including Parkinson’s disease and frontotemporal dementia. By merging early detection with targeted molecular intervention, Q-CETS represents a shift from reactive treatment to proactive, biology-guided neuromedicine.
References
- Barry, J. F., Schloss, J. M., Bauch, E., Turner, M. J., Hart, C. A., Pham, L. M., & Walsworth, R. L. (2020). Sensitivity optimization for nv-diamond magnetometry. Reviews of Modern Physics, 92(1). https://doi.org/10.1103/revmodphys.92.015004
- Chakraborty, A., Mohapatra, S. S., Barik, S., Roy, I., Gupta, B., & Biswas, A. (2023). Impact of nanoparticles on amyloid beta-induced Alzheimer’s disease, tuberculosis, leprosy and cancer: A systematic review. Bioscience Reports, 43(2). https://doi.org/10.1042/bsr20220324
- Chaparro, C. I. P., Simões, B. T., Borges, J. P., Castanho, M. A. R. B., Soares, P. I. P., & Neves, V. (2023). A promising approach: Magnetic nanosystems for Alzheimer’s disease theranostics. Pharmaceutics, 15(9), 2316. https://doi.org/10.3390/pharmaceutics15092316
- OpenAI. (2025). DALL·E (Version X) [Text-to-image model]. https://chat.openai.com/
- Fadul, S. M., Arshad, A., & Mehmood, R. (2023). CRISPR-based epigenome editing: Mechanisms and applications. Epigenomics, 15(21), 1137–1155. https://doi.org/10.2217/epi-2023-0281
- Gao, L., Wang, J., & Bi, Y. (2025). Nanotechnology for neurodegenerative diseases: Recent progress in brain-targeted delivery, stimuli-responsive platforms, and organelle-specific therapeutics. International Journal of Nanomedicine, Volume 20(11015-11044), 11015–11044. https://doi.org/10.2147/ijn.s549893
- Jack, C. R., Bennett, D. A., Blennow, K., Carrillo, M. C., Dunn, B., Haeberlein, S. B., Holtzman, D. M., Jagust, W., Jessen, F., Karlawish, J., Liu, E., Molinuevo, J. L., Montine, T., Phelps, C., Rankin, K. P., Rowe, C. C., Scheltens, P., Siemers, E., Snyder, H. M., & Sperling, R. (2018). NIA-AA research framework: Toward a biological definition of Alzheimer’s disease. Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, 14(4), 535–562. https://doi.org/10.1016/j.jalz.2018.02.018
- Kwak, G., Grewal, A., Hasan Slika, Mess, G., Li, H., Mohit Kwatra, Poulopoulos, A., Woodworth, G. F., Eberhart, C. G., Ko, H. S., Amir Manbachi, Caplan, J., Price, R. J., Tyler, B., & Suk, J. S. (2024). Brain nucleic acid delivery and genome editing via focused ultrasound-mediated blood–brain barrier opening and long-circulating nanoparticles. ACS Nano, 18(35), 24139–24153. https://doi.org/10.1021/acsnano.4c05270
- Meairs, S. (2015). Facilitation of drug transport across the blood–brain barrier with ultrasound and microbubbles. Pharmaceutics, 7(3), 275–293. https://doi.org/10.3390/pharmaceutics7030275
- National Institute on Aging. (2024, January 19). What happens to the brain in Alzheimer’s disease? National Institute on Aging. https://www.nia.nih.gov/health/alzheimers-causes-and-risk-factors/what-happens-brain-alzheimers-disease
- Selkoe, D. J., & Hardy, J. (2009). The amyloid hypothesis for Alzheimer’s disease: A critical reappraisal. Journal of Neurochemistry, 110(4), 1129–1134. https://doi.org/10.1111/j.1471-4159.2009.06181.x
- Tan, Y., Hu, X., Hou, Y., & Chu, Z. (2022). Emerging diamond quantum sensing in bio-membranes. Membranes, 12(10), 957. https://doi.org/10.3390/membranes12100957
- Zhang, Y., He, Z., Tong, X., Garrett, D. C., Cao, R., & Wang, L. V. (2024). Quantum imaging of biological organisms through spatial and polarization entanglement. Science Advances, 10(10). https://doi.org/10.1126/sciadv.adk1495
Other Course Work
📊 Assignment 1: EEG Analysis
📄 Psych 403_ Assignment 1_EEG_Filtering - Bani Sekhon.pdf
View Original PDFStep 1: 📥 Load brain wave data (like opening a music file, but for brain signals!)
Step 2: 📈 Create a plot showing 10 seconds of "raw" brain activity (all the noise included)
Step 3: 🔧 Apply a "filter" to clean up the signal (like noise-canceling headphones for data!)
Step 4: 📊 Make a side-by-side comparison (before vs after cleaning)
Step 5: 🌈 Create colorful "power spectrum" plots (shows which brain wave frequencies are strongest)
Visualizing Frequency Changes Over Time (Spectrogram)
🎨 Assignment 2: BrainImation
📄 NeuroStim - Assignment 2 - Bani Sekhon.pdf
View Original PDFAssignment 2 - Brainimation Art October 20, 2025
Tori and Bani
Original Code
// 🧠 BrainImation: Live EEG + P5.js
// Access real-time brain data through the 'eegData' object:
// eegData.alpha, eegData.beta, eegData.theta, eegData.delta
// eegData.attention, eegData.meditation, eegData.raw[]
let particles = [];
let time = 0 ;
function setup() {
// Canvas is already created by the system
// Just set up the drawing mode and initialize
colorMode( HSB , 360 , 100 , 100 , 1 );
// Initialize particles
for ( let i = 0 ; i < 50 ; i++) {
particles.push({
x: random(width),
y: random(height),
vx: random(- 1 , 1 ),
vy: random(- 1 , 1 ),
hue: random( 360 )
});
}
}
function draw() {
// Background responds to meditation
let bgAlpha = map(eegData.meditation, 0 , 1 , 0.05 , 0.2 );
background( 220 , 30 , 10 , bgAlpha);
time += 0.01 ;
// Draw neural network
stroke( 180 , 80 , 90 , 0.3 );
strokeWeight( 1 );
for ( let i = 0 ; i < particles.length; i++) {
let p = particles[i];
// Movement influenced by alpha waves
let alphaForce = eegData.alpha * 2 ;
p.vx += random(-alphaForce, alphaForce) * 0.01 ;
p.vy += random(-alphaForce, alphaForce) * 0.01 ;
// Damping
p.vx *= 0.99 ;
p.vy *= 0.99 ;
// Update position
p.x += p.vx;
p.y += p.vy;
// Wrap around edges
if (p.x < 0 ) p.x = width;
if (p.x > width) p.x = 0 ;
if (p.y < 0 ) p.y = height;
if (p.y > height) p.y = 0 ;
// Color influenced by attention
let hue = (p.hue + eegData.attention * 50 + time * 10 ) % 360 ;
let brightness = map(eegData.beta, 0 , 1 , 30 , 90 );
fill(hue, 70 , brightness, 0.8 );
noStroke();
// Size influenced by theta waves
let size = 5 + eegData.theta * 15 ;
ellipse(p.x, p.y, size);
// Connect nearby particles
for ( let j = i + 1 ; j < particles.length; j++) {
let p2 = particles[j];
let d = dist(p.x, p.y, p2.x, p2.y);
if (d < 80 ) {
let alpha = map(d, 0 , 80 , 0.5 , 0 ) * eegData.alpha;
stroke(hue, 50 , 70 , alpha);
strokeWeight( 1 );
line(p.x, p.y, p2.x, p2.y);
}
}
}
// Display connection status
if (!eegData.connected) {
fill( 0 , 0 , 100 , 0.8 );
textAlign( CENTER , CENTER );
textSize( 20 );
text( "Connect your Muse headset or use 'Simulate Data'" , width/ 2 , height/ 2 - 10 );
textSize( 16 );
fill( 0 , 0 , 70 , 0.6 );
text( "to see brain-controlled animation" , width/ 2 , height/ 2 + 20 );
}
}
Steps
1. Converted the original code into a kaleidoscope shape using ChatGPT
2. Colors and movement respond to brain wavesIncreased pulse size depending on which type of
brain wave is coming in
3. Gave each brain wave its own corresponding colour; Alpha/Theta = Blue, Beta = Orange/Red,
Delta = White
4. Then the code only showed one colour and did not change depending on wave type, so the code
was edited to only include the simulated data as it was trying to incorporate the MUSE data at the
same time (which was not present). Then at the end of the code “ text("to see brain-controlled
kaleidoscope", 0, 20)” was added to specify the action.
5. We then asked the code to pulse when brain waves of the same type meet/collide, to create a wave
specific connection system.
Purpose of this Code
We created a code that would reflect a kaleidoscope based on the real-time brain data. We wanted the
alpha and theta waves to reflect calm colours like blue and cyan (brain waves that are more evident during
meditation and focus), the beta waves to reflect more chaotic colours like red and orange (brain waves
that are more evident during anxiety-inducing situations), and the delta waves to reflect the colour white
(brain waves that are more evident during deep sleep).
Final Code:
// EEG-Responsive Kaleidoscope with Wave-Specific Pulsing Connections and Size Growth
let particles = [];
let time = 0 ;
let symmetry = 6 ;
let angle = TWO_PI / symmetry;
function setup() {
colorMode( HSB , 360 , 100 , 100 , 1 );
// Initialize particles with wave group (0=Alpha, 1=Theta, 2=Beta, 3=Delta)
for ( let i = 0 ; i < 50 ; i++) {
particles.push({
x: random(width),
y: random(height),
vx: random(- 1 , 1 ),
vy: random(- 1 , 1 ),
hue: random( 360 ),
saturation: 80 ,
size: 5 ,
waveGroup: i % 4
});
}
}
function draw() {
// Background responds to meditation
background( 220 , 30 , 10 , map(eegData.meditation, 0 , 1 , 0.05 , 0.2 ));
translate(width / 2 , height / 2 );
time += 0.01 ;
for ( let i = 0 ; i < particles.length; i++) {
let p = particles[i];
// Wave amplitudes
let alpha = eegData.alpha;
let theta = eegData.theta;
let beta = eegData.beta;
let delta = eegData.delta;
// Particle movement influenced by waves
let moveForce = (alpha + theta)* 2 + beta* 2 + delta;
p.vx += random(-moveForce, moveForce) * 0.01 ;
p.vy += random(-moveForce, moveForce) * 0.01 ;
p.vx *= 0.99 ;
p.vy *= 0.99 ;
p.x += p.vx;
p.y += p.vy;
// Wrap around edges
if (p.x < 0 ) p.x = width;
if (p.x > width) p.x = 0 ;
if (p.y < 0 ) p.y = height;
if (p.y > height) p.y = 0 ;
let cx = p.x - width / 2 ;
let cy = p.y - height / 2 ;
// --- Assign wave-specific color ---
let targetHue, targetSaturation, targetBrightness;
if (p.waveGroup === 0 ) {
targetHue = map(alpha, 0 , 1 , 180 , 220 ); // Alpha - Blue
targetSaturation = 80 ;
targetBrightness = 80 ;
} else if (p.waveGroup === 1 ) {
targetHue = map(theta, 0 , 1 , 200 , 240 ); // Theta - Cyan
targetSaturation = 80 ;
targetBrightness = 80 ;
} else if (p.waveGroup === 2 ) {
targetHue = map(beta, 0 , 1 , 0 , 30 ); // Beta - Red/Orange
targetSaturation = 100 ;
targetBrightness = 80 ;
} else {
targetHue = 0 ; // Delta - White
targetSaturation = 0 ;
targetBrightness = map(delta, 0 , 1 , 50 , 100 );
}
// Smooth color transitions
p.hue = lerp(p.hue, targetHue, 0.05 );
p.saturation = lerp(p.saturation, targetSaturation, 0.05 );
let brightness = targetBrightness;
// --- Particle size based on wave ---
let targetSize;
if (p.waveGroup === 0 ) targetSize = 5 + alpha * 15 ;
else if (p.waveGroup === 1 ) targetSize = 5 + theta * 15 ;
else if (p.waveGroup === 2 ) targetSize = 5 + beta * 15 ;
else targetSize = 5 + delta * 15 ;
p.size = lerp(p.size, targetSize, 0.1 );
// --- Draw particle in kaleidoscope symmetry ---
for ( let s = 0 ; s < symmetry; s++) {
rotate(angle);
fill(p.hue, p.saturation, brightness, 0.8 );
noStroke();
ellipse(cx, cy, p.size);
push();
scale( 1 , - 1 );
ellipse(cx, cy, p.size);
pop();
}
// --- Wave-specific connections with pulsing and size growth ---
for ( let j = i + 1 ; j < particles.length; j++) {
let p2 = particles[j];
// Connect only particles of the same wave group
if (p.waveGroup !== p2.waveGroup) continue ;
let dx = p2.x - width / 2 ;
let dy = p2.y - height / 2 ;
let d = dist(cx, cy, dx, dy);
if (d < 80 ) {
// Wave amplitude
let waveAmp;
if (p.waveGroup === 0 ) waveAmp = alpha;
else if (p.waveGroup === 1 ) waveAmp = theta;
else if (p.waveGroup === 2 ) waveAmp = beta;
else waveAmp = delta;
// Pulsing effect
let pulse = map(sin(time * 5 ), - 1 , 1 , 0.3 , 1 );
let alphaLine = map(d, 0 , 80 , 0.5 , 0 ) * waveAmp * pulse;
// Increase particle size on connection
let sizeBoost = map(d, 0 , 80 , waveAmp * 5 , 0 );
p.size = lerp(p.size, p.size + sizeBoost, 0.2 );
p2.size = lerp(p2.size, p2.size + sizeBoost, 0.2 );
// Optional subtle hue shift for pulse
let pulseHue = p.hue + pulse * 10 ;
stroke(pulseHue, p.saturation * 0.7 , brightness * 0.7 , alphaLine);
strokeWeight( 1 + waveAmp * 2 );
// Kaleidoscope rotation
for ( let s = 0 ; s < symmetry; s++) {
rotate(angle);
line(cx, cy, dx, dy);
push();
scale( 1 , - 1 );
line(cx, cy, dx, dy);
pop();
}
}
}
}
// --- Message for simulated EEG data ---
if (!eegData.connected) {
fill( 0 , 0 , 100 , 0.8 );
textAlign( CENTER , CENTER );
textSize( 20 );
text( "Using simulated EEG data" , 0 , - 10 );
textSize( 16 );
fill( 0 , 0 , 70 , 0.6 );
text( "Colors and movement respond to brain waves" , 0 , 20 );
}
}
Challenges Faced:
We were unable to connect our muse headband, so simulated data was used
We could not get the kaleidoscope P5.js code to work in the brainanimation system. After repeated attempts
we figured out it was due to the code being meant for a mouse and would not work for what we wanted. We
created our own kaleidoscope design using ChatGTP, that would respond to the EEG brainwave data.
Changing the colours within the code was also challenging as it kept combining the colours together. This was
solved through increased specificity and lots of trial and error.
Screenshots
🎯 Midterm Project
📄 Sekhon, Bani, 1757205 - Bani Sekhon.pdf
View Original PDF(Part 1) Extend your Assignment 2 BrainImation project with novel BCI concepts
Description :
For this project, I implemented a novel Brain-Computer Interface (BCI) concept that dynamically visualizes a user’s
mental state through a kaleidoscope display. The system translates real-time brainwave activity into changes in both
color and intensity, creating a visually intuitive representation of the user’s cognitive and emotional state. Unlike
traditional BCI applications that focus on basic parameter control (such as moving a cursor or adjusting a single
variable), this implementation provides a multi-dimensional, immersive feedback loop, combining visual aesthetics
with cognitive monitoring.
The logic of the system operates on a continuous loop. Brainwave data is collected and analyzed to determine the
relative power of alpha, theta, and beta frequencies. When alpha and theta waves dominate, frequencies commonly
associated with relaxation and calmness, the kaleidoscope shifts toward cool tones, such as blues and cyans.
Conversely, when beta waves are predominant, indicating stress or heightened cognitive load, warmer colors like
reds and oranges become more prominent. The display also includes a textual indicator at the top, stating whether
the user is “Relaxed,” “Focused,” or “Stressed,” based on the detected brainwave pattern. This real-time mapping of
mental state to visual output allows the user to immediately perceive their cognitive and emotional status in an
intuitive and engaging way.
What sets this BCI apart from basic parameter control is its emphasis on continuous, multi-sensory feedback rather
than simple binary outputs or single-variable adjustments. The system does not merely respond to one input; it
interprets a combination of brainwave frequencies and translates them into both color gradients and text, creating a
rich, interactive visualization. This approach highlights the potential of BCIs for more expressive and artistic
applications, rather than purely functional ones.
Implementing this system taught me the importance of real-time signal processing, the subtlety of mapping abstract
neural signals to intuitive visual feedback, and the challenge of designing an interface that is both responsive and
aesthetically meaningful. It reinforced the idea that BCIs can serve as tools not just for control, but for enhancing
self-awareness and engagement with one’s own cognitive and emotional states.
Screen Recording:
(2) Create an Event-Related Potential (ERP) experiment using BrainImation.
Description :
The ERP component measured in this experiment is the P300 (or P3b), a positive deflection in EEG that typically
occurs 300–600 milliseconds after a rare or meaningful stimulus. The P300 reflects attentional resource allocation
and stimulus evaluation, rather than the physical features of the stimulus, and is one of the most widely studied
cognitive ERP components. Its amplitude and latency vary with factors such as stimulus probability, task relevance,
and participant age (as shown in studies summarized in P300 Development Across the Lifespan: A Systematic
Review and Meta-Analysis ).
This project implements a visual oddball paradigm using simulated EEG data. Two stimulus categories are
presented: a frequent standard stimulus (blue circle; 80% probability) and a rare target stimulus (red circle; 20%
probability). Each trial triggers an EEG epoch representing a –200 ms baseline period and an 800 ms post-stimulus
window. The simulation adds a positive-going deflection around 300–600 ms for rare trials to mimic the real P300
response observed in human EEG data. The system separately averages epochs for standard and rare stimuli,
displaying both on the same ERP plot (blue vs. red) with labeled axes, timing markers, and trial counters for each
condition.
Two versions of the experiment were implemented.
The first version provides the core functionality with a 1-second epoch and straightforward averaging—ideal for
clear visualization and demonstration.
The second version extends the epoch length to approximately 1.5 seconds (–200 to +800 ms) and introduces
baseline correction, in which the mean of the pre-stimulus samples (–200 to 0 ms) is subtracted from the entire
epoch. This adjustment ensures that the averaged waveform reflects relative changes following stimulus onset rather
than absolute voltage shifts.
If conducted with real EEG, consistent with classic findings by Sutton et al. (1965), we would expect the rare targets
to elicit a larger and delayed positive peak around 300–600 ms over parietal electrodes, while frequent standards
would show minimal or no such positivity.
Screen Recording Version 1:
Screen Recording Version 2:
📝 Sekhon_Midterm_Part1 - Bani Sekhon.txt
💡 Code is embedded in this portfolio - opens instantly in the live BrainImation editor (no internet required!)
📝 Sekhon_Midterm_Part2a - Bani Sekhon.txt
💡 Code is embedded in this portfolio - opens instantly in the live BrainImation editor (no internet required!)
📝 Sekhon_Midterm_Part2b - Bani Sekhon.txt
💡 Code is embedded in this portfolio - opens instantly in the live BrainImation editor (no internet required!)