Abstract: Dr. Zawawi Abdullah — MAAFIM 6th International Conference 2026

Presentation Abstract

Strategies for Cognitive Rejuvenation via Senolysis, Brain Peptides and Bioregulator Therapy

Day 3 · 22nd August 2026 · 2:45 PM

Abstract:

Cognitive decline associated with aging is increasingly recognized as a consequence of the progressive accumulation of senescent cells (SnCs) within the neurovascular and neuronal niches. These SnCs establish a pro-inflammatory secretory phenotype (SASP) that impairs the function of the endogenous neural stem cell (NSC) pool, effectively “fortifying” the brain against endogenous regenerative processes.

The accumulation of senescent cells acts as a structural and biochemical barrier to neurogenesis, preventing NSCs from differentiating and integrating into mature neural circuits. The targeted elimination of these cells, or “senolysis,” offers a therapeutic strategy to clear this barrier and restore the regenerative capacity of the brain. Procyanidin C1 (PCC1) has emerged as a potent senotherapeutic agent that can selectively induce apoptosis in senescent cells, thereby facilitating a rejuvenate microenvironment.

Intervention:

Beyond senolytic clearance, cognitive improvement may be achieved through the targeted use of neuropeptides and bioregulators.

Pharmacological agents such as Semax, Selank, Cerebrolysin, and Cortexin have demonstrated efficacy in promoting neuroplasticity, enhancing synaptic transmission, and supporting overall cognitive performance. Complementing these are bioregulator peptides—including Epithalon, Pinealon, and Thymosin Alpha-1—which operate through direct and indirect pathways to optimize genetic expression, modulate immune homeostasis, and promote neuroprotection.

Summary:

A triple-modality approach—integrating senolytic clearance (e.g., via PCC1) to remove regenerative blockades, followed by the administration of neuro-active peptides and bioregulators—represents a promising integrative strategy to mitigate age-related cognitive decline and restore neurological homeostasis.

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