Panos Zanos

Mar 17, 2025 | biorxiv.org | Andrea Georgiou |Panos Zanos |Anna Onisiforou

AbstractAlzheimer′s disease (AD) and Diabetes Mellitus Type II (DM2) share overlapping pathological mechanisms, with DM2 increasing AD risk. Disease-modifying therapies (DMTs) for DM2, including Metformin and Semaglutide, have been explored for neuroprotection, yet their efficacy in AD remains unclear.

Jan 5, 2025 | mdpi.com | Panos Zanos

1. IntroductionAlzheimer’s Disease (AD) is a progressive and chronic neurodegenerative disease (ND) affecting the central nervous system (CNS), marked primarily by memory loss and cognitive deterioration []. Conventional treatments offer symptomatic relief, but no pharmacotherapies have yet been able to halt or reverse its progression []. AD is the most common type of dementia among older adults, impacting approximately 55 million individuals globally [].

Jul 15, 2024 | pharmrev.aspetjournals.org | Panos Zanos |Ruin Moaddel |Patrick Morris |Lace M. Riggs

AbstractKetamine, a racemic mixture consisting of (S)- and (R)-ketamine, has been in clinical use since 1970. Although best characterized for its dissociative anesthetic properties, ketamine also exerts analgesic, anti-inflammatory, and antidepressant actions. We provide a comprehensive review of these therapeutic uses, emphasizing drug dose, route of administration, and the time course of these effects.

Jul 3, 2024 | sciencedirect.com | A. Auerbach |Panos Zanos |Todd Gould |Yoshifumi Okochi

Despite the importance of speed in synaptic transmission, in many synapses, neurotransmitters bind to their receptors at rates that appear to be slower than the diffusion limit. This assessment is generally based on a comparison with the Smoluchowski limit rather than an independent experimental analysis. In many synapses, miniature excitatory postsynaptic currents (mEPSCs) are controlled by the interplay between binding to receptors and diffusion of the neurotransmitter out of the synaptic cleft.

Jun 26, 2024 | nature.com | Anna Onisiforou |Panos Zanos |Polymnia Georgiou

Major depressive disorder (MDD) and substance-use disorders (SUDs) often lead to premature aging, increasing vulnerability to cognitive decline and other forms of dementia. This study utilized advanced systems bioinformatics to identify aging “signatures” in MDD and SUDs and evaluated the potential for known lifespan-extending drugs to target and reverse these signatures. The results suggest that inhibiting the transcriptional activation of FOS gene family members holds promise in mitigating premature aging in MDD and SUDs. Conversely, antidepressant drugs activating the PI3K/Akt/mTOR pathway, a common mechanism in rapid-acting antidepressants, may accelerate aging in MDD patients, making them unsuitable for those with comorbid aging-related conditions like dementia and Alzheimer’s disease. Additionally, this innovative approach identifies potential anti-aging interventions for MDD patients, such as Deferoxamine, Resveratrol, Estradiol valerate, and natural compounds like zinc acetate, genistein, and ascorbic acid, regardless of comorbid anxiety disorders. These findings illuminate the premature aging effects of MDD and SUDs and offer insights into treatment strategies for patients with comorbid aging-related conditions, including dementia and Alzheimer’s disease.