Goto

Collaborating Authors

 alzheimer




He Went to Prison for Gene-Editing Babies. Now He's Planning to Do It Again

WIRED

He Went to Prison for Gene-Editing Babies. Now He's Planning to Do It Again Chinese scientist He Jiankui wants to end Alzheimer's and thinks Silicon Valley is conducting a "Nazi eugenic experiment." In 2018, a nervous-looking He Jiankui took the stage at a scientific conference in Hong Kong. A hush settled over the packed auditorium as the soft-spoken Chinese scientist adjusted his microphone and confirmed the circulating media reports: He had created the world's first gene-edited babies . Three little girls were born with modifications to their genomes that were intended to protect them against HIV. The changes he'd made to their DNA were permanent and heritable, meaning they could be passed down to future generations.


Reinforcement Learning based Disease Progression Model for Alzheimer's Disease

Neural Information Processing Systems

DEs provide relationships between some, but not all, factors relevant to AD. We assume that the missing relationships must satisfy general criteria about the working of the brain, for e.g., maximizing cognition while minimizing the cost of supporting cognition. This allows us to extract the missing relationships by using RL to optimize an objective (reward) function that captures the above criteria. We use our model consisting of DEs (as a simulator) and the trained RL agent to predict individualized 10-year AD progression using baseline (year 0) features on synthetic and real data. The model was comparable or better at predicting 10-year cognition trajectories than state-of-the-art learning-based models. Our interpretable model demonstrated, and provided insights into, recovery/compensatory processes that mitigate the effect of AD, even though those processes were not explicitly encoded in the model. Our framework combines DEs with RL for modelling AD progression and has broad applicability for understanding other neurological disorders.


Data Holds the Key in Slowing Age-Related Illnesses

WIRED

More accurate and individualized health predictions will allow for preventative factors to be implemented well in advance. In 2026, we will see the beginning of precision medical forecasting. Just as there have been remarkable advances in weather forecasting with the use of large language models, so will there be for determining an individual's risk of the major age-related diseases (cancer, cardiovascular, and neurodegenerative). These diseases share common threads, such as a long incubation phase before any symptoms are manifest, usually two decades or more. They also have the same biologic underpinnings of immunosenescence and inflammaging, terms that characterize an immune system that has lost some of its functionality and protective power, and the accompanying heightened inflammation.


Brie, cheddar, and other high-fat cheeses linked to lower dementia risk

Popular Science

Breakthroughs, discoveries, and DIY tips sent every weekday. It's been found in ancient human feces . The U.S. government stored 6.4 metric tons of it in mountains . And a big hunk of it played a major role in a presidential farewell party . While too much of the popular dairy product can spell tummy troubles and high cholesterol for some, new research suggests that eating more high-fat cheese and cream could be linked to a lower risk of developing dementia .


Domain-Specific Foundation Model Improves AI-Based Analysis of Neuropathology

Verma, Ruchika, Kandoi, Shrishtee, Afzal, Robina, Chen, Shengjia, Jegminat, Jannes, Karlovich, Michael W., Umphlett, Melissa, Richardson, Timothy E., Clare, Kevin, Hossain, Quazi, Samanamud, Jorge, Faust, Phyllis L., Louis, Elan D., McKee, Ann C., Stein, Thor D., Cherry, Jonathan D., Mez, Jesse, McGoldrick, Anya C., Mora, Dalilah D. Quintana, Nirenberg, Melissa J., Walker, Ruth H., Mendez, Yolfrankcis, Morgello, Susan, Dickson, Dennis W., Murray, Melissa E., Cordon-Cardo, Carlos, Tsankova, Nadejda M., Walker, Jamie M., Dangoor, Diana K., McQuillan, Stephanie, Thorn, Emma L., De Sanctis, Claudia, Li, Shuying, Fuchs, Thomas J., Farrell, Kurt, Crary, John F., Campanella, Gabriele

arXiv.org Artificial Intelligence

Foundation models have transformed computational pathology by providing generalizable representations from large-scale histology datasets. However, existing models are predominantly trained on surgical pathology data, which is enriched for non-nervous tissue and overrepresents neoplastic, inflammatory, metabolic, and other non-neurological diseases. Neuropathology represents a markedly different domain of histopathology, characterized by unique cell types (neurons, glia, etc.), distinct cytoarchitecture, and disease-specific pathological features including neurofibrillary tangles, amyloid plaques, Lewy bodies, and pattern-specific neurodegeneration. This domain mismatch may limit the ability of general-purpose foundation models to capture the morphological patterns critical for interpreting neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and cerebellar ataxias. To address this gap, we developed NeuroFM, a foundation model trained specifically on whole-slide images of brain tissue spanning diverse neurodegenerative pathologies. NeuroFM demonstrates superior performance compared to general-purpose models across multiple neuropathology-specific downstream tasks, including mixed dementia disease classification, hippocampal region segmentation, and neurodegenerative ataxia identification encompassing cerebellar essential tremor and spinocerebellar ataxia subtypes. This work establishes that domain-specialized foundation models trained on brain tissue can better capture neuropathology-specific features than models trained on general surgical pathology datasets. By tailoring foundation models to the unique morphological landscape of neurodegenerative diseases, NeuroFM enables more accurate and reliable AI-based analysis for brain disease diagnosis and research, setting a precedent for domain-specific model development in specialized areas of digital pathology.


Physics-Informed Neural Koopman Machine for Interpretable Longitudinal Personalized Alzheimer's Disease Forecasting

Hrusanov, Georgi, Vu, Duy-Thanh, Can, Duy-Cat, Tascedda, Sophie, Ryan, Margaret, Bodelet, Julien, Koscielska, Katarzyna, Magnus, Carsten, Chén, Oliver Y.

arXiv.org Artificial Intelligence

Early forecasting of individual cognitive decline in Alzheimer's disease (AD) is central to disease evaluation and management. Despite advances, it is as of yet challenging for existing methodological frameworks to integrate multimodal data for longitudinal personalized forecasting while maintaining interpretability. To address this gap, we present the Neural Koopman Machine (NKM), a new machine learning architecture inspired by dynamical systems and attention mechanisms, designed to forecast multiple cognitive scores simultaneously using multimodal genetic, neuroimaging, proteomic, and demographic data. NKM integrates analytical ($α$) and biological ($β$) knowledge to guide feature grouping and control the hierarchical attention mechanisms to extract relevant patterns. By implementing Fusion Group-Aware Hierarchical Attention within the Koopman operator framework, NKM transforms complex nonlinear trajectories into interpretable linear representations. To demonstrate NKM's efficacy, we applied it to study the Alzheimer's Disease Neuroimaging Initiative (ADNI) dataset. Our results suggest that NKM consistently outperforms both traditional machine learning methods and deep learning models in forecasting trajectories of cognitive decline. Specifically, NKM (1) forecasts changes of multiple cognitive scores simultaneously, (2) quantifies differential biomarker contributions to predicting distinctive cognitive scores, and (3) identifies brain regions most predictive of cognitive deterioration. Together, NKM advances personalized, interpretable forecasting of future cognitive decline in AD using past multimodal data through an explainable, explicit system and reveals potential multimodal biological underpinnings of AD progression.


Can AI Look at Your Retina and Diagnose Alzheimer's? Eric Topol Hopes So

WIRED

Can AI Look at Your Retina and Diagnose Alzheimer's? The author of believes AI could bring big changes to the world of medicine. For decades now, it's been fairly well established that once you turn 40 you should start paying more attention to your body. That's when women are supposed to start getting mammograms and men are supposed to start paying a bit more attention to their prostates. Over the next decade, you'll start getting colonoscopies, and from then on out, it feels like a gradual march of doctor's appointments and tests until your body collapses sometime in your seventies or eighties.


xEEGNet: Towards Explainable AI in EEG Dementia Classification

Zanola, Andrea, Tshimanga, Louis Fabrice, Del Pup, Federico, Baiesi, Marco, Atzori, Manfredo

arXiv.org Artificial Intelligence

This work presents xEEGNet, a novel, compact, and explainable neural network for EEG data analysis. It is fully interpretable and reduces overfitting through major parameter reduction. As an applicative use case, we focused on classifying common dementia conditions, Alzheimer's and frontotemporal dementia, versus controls. xEEGNet is broadly applicable to other neurological conditions involving spectral alterations. We initially used ShallowNet, a simple and popular model from the EEGNet-family. Its structure was analyzed and gradually modified to move from a "black box" to a more transparent model, without compromising performance. The learned kernels and weights were examined from a clinical standpoint to assess medical relevance. Model variants, including ShallowNet and the final xEEGNet, were evaluated using robust Nested-Leave-N-Subjects-Out cross-validation for unbiased performance estimates. Variability across data splits was explained using embedded EEG representations, grouped by class and set, with pairwise separability to quantify group distinction. Overfitting was assessed through training-validation loss correlation and training speed. xEEGNet uses only 168 parameters, 200 times fewer than ShallowNet, yet retains interpretability, resists overfitting, achieves comparable median performance (-1.5%), and reduces variability across splits. This variability is explained by embedded EEG representations: higher accuracy correlates with greater separation between test set controls and Alzheimer's cases, without significant influence from training data. xEEGNet's ability to filter specific EEG bands, learn band-specific topographies, and use relevant spectral features demonstrates its interpretability. While large deep learning models are often prioritized for performance, this study shows smaller architectures like xEEGNet can be equally effective in EEG pathology classification.