Longitudinal tracking of dyadic body temperature synchrony in social pairs across species.

Alzheimer’s disease (AD) is a progressive neurological disorder manifesting with memory complaints and cognitive decline [–]. It is the most common cause of dementia and the seventh leading cause of death worldwide []. AD is linked to the accumulation of amyloid β (Aβ) plaques, which leads to extracellular senile amyloid plaques and hyperphosphorylated tau protein deposition, leading to intraneuronal neurofibrillary tangles [, –]. In addition to the mentioned characteristic pathological hallmarks of AD, loss of synaptic plasticity, synaptic loss, and neuronal loss play a role in the neuropathology of AD [, , ]. Monoclonal antibodies (mAbs) have presented unique therapeutic opportunities for treating AD. They play a crucial role in targeting specific disease-related proteins, such as Aβ and tau, which are hallmarks of AD pathology [–]. However, the effective delivery of mAbs to the brain remains a significant challenge due to the presence of the blood–brain barrier (BBB) [, ]. The BBB is a highly selective and tightly regulated barrier that controls the flow of molecules between the blood and the brain []. It serves to maintain the homeostasis of the brain and protect it from harmful substances []. In Alzheimer’s disease, this protective function represents a major barrier to effective delivery of mAbs and other disease-modifying agents, thereby limiting therapeutic exposure at target sites [].