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L. Gaetani

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Jul 2026

Can the integration of blood-based biomarkers into Alzheimer's disease diagnosis revolutionize the field?

INTRODUCTION Alzheimer's disease (AD) is a clinical-biological entity in which pathophysiological changes precede symptoms by years. Biomarkers are essential for early and accurate diagnosis, particularly in the era of disease-modifying therapies requiring biological confirmation. Cerebrospinal fluid (CSF) and amyloid positron emission tomography (amyloid-PET) are the reference standards, but increasing attention is devoted to blood-based biomarkers (BBMs) due to their scalability and cost-effectiveness. AREAS COVERED In this critical perspective, the authors critically appraise the current evidence supporting plasma phosphorylated tau at threonine 217 (p-tau217) as the leading BBM for AD. They also discuss its analytical performance, biological rationale, and diagnostic accuracy across the AD continuum, its relationship with established CSF, PET, and neuropathological biomarkers, its potential role in identifying patients eligible for disease-modifying therapies, and the main clinical and biological factors influencing its interpretation. Finally, they highlight current limitations, unresolved challenges, and give their future perspectives for the integration of plasma biomarkers into routine clinical practice. EXPERT OPINION BBMs are expected to reshape AD diagnostics. A stepwise approach, using plasma biomarkers as first-line tests followed by confirmatory CSF or PET, is currently the most feasible strategy. Ultimately, highly specific, brain-derived tau biomarkers may enable BBMs to replace CSF biomarkers.

L. Gaetani, Giovanna Nardi, Lucilla Parnetti · 0 citations
Review Open access Aug 2026

Thalamocortical connectivity and nucleus-specific thalamic dysfunction in temporal lobe epilepsy: an integrative review

Temporal lobe epilepsy (TLE) is increasingly recognized as a distributed network disorder extending beyond mesial temporal structures. Among the brain regions implicated in epileptic network organization, the thalamus has emerged as a key hub due to its extensive structural and functional connections with cortical, limbic, and subcortical systems.This integrative review aimed to synthesize current evidence regarding nucleus-specific thalamic abnormalities and thalamocortical connectivity alterations in TLE.A literature search was conducted following PRISMA guidelines using PubMed and Google Scholar databases. Twenty-eight studies were included in the qualitative synthesis, with nineteen studies providing detailed nucleus-specific structural, functional, or electrophysiological characterization of thalamic involvement.Across structural MRI, diffusion imaging, resting-state functional MRI, magnetoencephalography, and stereo-electroencephalography studies, convergent evidence indicated preferential involvement of the anterior thalamic nucleus (ANT), mediodorsal nucleus (MD), pulvinar, and intralaminar nuclei. TLE with mesial temporal sclerosis generally exhibited more extensive thalamic atrophy and thalamotemporal disconnection, whereas MRI-negative TLE showed more heterogeneous functional and network-level abnormalities. Electrophysiological studies demonstrated dynamic thalamic participation in seizure propagation and network synchronization, supporting an active role of thalamic nuclei in epileptic processes. Emerging longitudinal evidence further suggests that thalamocortical networks may undergo postoperative reorganization following successful epilepsy surgery.Overall, the available evidence supports a transition from a predominantly hippocampocentric framework toward a distributed thalamocortical network model of TLE. Nucleus-specific thalamic dysfunction appears to contribute to seizure propagation, cognitive impairment, and large-scale network dysregulation, highlighting the importance of multimodal approaches for understanding epileptic network organization.

Giuseppina Bevacqua, Marco Ciavarro, L. Gaetani et al. · 0 citations