Mild Cognitive Impairment is a critical early stage of cognitive decline that frequently precedes Alzheimer's disease, yet its automated detection from neuropsychological drawing tests remains fundamentally constrained by data scarcity, class imbalance, and diagnostic ambiguity near clinical boundaries. Existing methodologies attempt to bypass these constraints using computationally expensive, fully fine-tuned hybrid architectures that relegate spatial explainability to a post-hoc approximation rather than an intrinsic model property. We propose a parameter-efficient framework utilizing frozen DINOv2-Small model adapted via three modality-specific learnable prompt tokens while Operating with 1.19 million trainable parameters, each token serves as a query in a shared cross-attention layer over the source image patch tokens. Crucially, spatial explainability is achieved directly through these attention maps; as a structural consequence of the architecture. Then task-conditioned embeddings fused via an attention module to quantify modality-level importance per subject. To handle boundary ambiguity, a MoCA-adapted focal loss introduced that integrates continuous cognitive scores into the training target, loss modulation, and adaptive sample weighting, strictly generalizing standard soft-label approaches. Under stratified five-fold cross-validation, the proposed architecture yields an MCI-class F1 of 0.641 and an AUC of 0.795, outperforming the computationally heavier ResViT baseline by 0.110 in MCI-class F1.
Background: Graph neural networks improve computational prediction of polypharmacy side effects, but standard binary cross-entropy training allocates equal capacity to well-classified and difficult examples, potentially missing clinically significant interactions. We evaluated whether an asymmetric focal objective could improve multi-relational drug-drug interaction (DDI) prediction by emphasizing difficult positive interactions. Methods: ClinicalFocal loss was integrated into a relation-aware graph convolutional network using molecular fingerprints, physicochemical descriptors, and learned embeddings. The model was evaluated on TWOSIDES using five-fold cross-validation with identical experimental conditions (architecture, features, data partitions, hyperparameters, and random seeds) for ClinicalFocal loss and binary cross-entropy baseline. Results: ClinicalFocal loss increased accuracy from 0.699 to 0.892 (+19.3 percentage points) and F1 score from 0.700 to 0.894 (+19.4 percentage points). AUROC increased from 0.766 to 0.914, and AUCPR increased from 0.714 to 0.860. The false-negative rate decreased from 29.8% to 9.1%, while specificity increased from 69.6% to 87.5%. Overall classification error decreased from 30.1% to 10.8%, corresponding to a 64.1% relative reduction. Improvements were consistent across all five folds. Conclusions: Asymmetric focal optimization improved classification and ranking performance while achieving 90.9% recall for observed interaction triples, without modifying the underlying architecture. Loss-function design is a direct, tunable lever for improving graph-based DDI prediction.