This review examines the roles and mechanisms of Wnt signaling in Alzheimer’s disease (AD). AD is pathologically defined by extracellular amyloid-β (Aβ) plaque deposition and neurofibrillary tangles composed of hyperphosphorylated tau, accompanied by synaptic loss, neuroinflammation, blood–brain barrier (BBB) dysfunction, and progressive brain atrophy. Growing evidence identifies Wnt signaling as a central regulatory system that maintains neuronal survival, synaptic plasticity, and neurovascular unit homeostasis. Disruption of Wnt signaling intersects with and amplifies AD pathology at multiple levels. Attenuated Wnt activity can derepress amyloidogenic pathways, including BACE1 expression, and compromise cellular environments that support Aβ clearance. Aberrant activation of glycogen synthase kinase-3β (GSK-3β) promotes tau hyperphosphorylation, while altered Wnt-dependent synaptic protein homeostasis and excitatory–inhibitory balance destabilize neuronal networks. In parallel, Wnt signaling modulates microglial and astrocytic inflammatory state transitions and contributes to BBB integrity and repair. Key regulators—including LRP5/6, LRP1, the Dickkopf (DKK) family (particularly DKK1 and the atypical DKK3), sFRP1, Kremen, Notum, and R-spondins—collectively shape Wnt signal strength, receptor availability, and antagonistic tone, forming a pathogenic network characterized by receptor gating, antagonist amplification, and clearance cross-talk. We summarize three major Wnt-oriented therapeutic strategies: enhancing canonical Wnt/β-catenin signaling, reducing antagonistic pressure on Wnt receptors, and modulating LRP family functions to coordinate synaptic protection, BBB repair, and Aβ clearance. Overall, Wnt signaling represents a promising disease-modifying axis centered on synaptic and network resilience; however, successful clinical translation will require refined understanding of cell-type specificity, disease-stage dependence, context-dependent effects of regulators such as DKK3, and the development of robust pharmacodynamic biomarkers.

Traumatic brain injury (TBI) initiates a cascade of secondary molecular and cellular events that drive long-term neurological dysfunction. Increasing evidence positions epigenetic regulation as a central integrative mechanism through which acute injury-related signals are translated into sustained alterations in gene expression, cell state, and circuit function. Epigenetic mechanisms—including DNA methylation, histone modifications, and non-coding RNAs—act in a coordinated, cell type–specific manner to shape transcriptional programs underlying neuroinflammation, synaptic remodeling, and behavioral outcomes after TBI. Recent advances in epigenomic and transcriptomic profiling, particularly single-cell, spatial, and integrative multi-omics approaches, have enabled systems-level interrogation of injury-induced regulatory networks across neurons, glia, and the neurovascular unit. Beyond mechanistic insight, epigenetic reprogramming provides a conceptual framework for biomarker discovery and therapeutic development, given the accessibility and reversibility of epigenetic states. This review synthesizes current evidence to highlight how epigenetic mechanisms link acute brain injury to chronic neurological sequelae and discusses emerging opportunities for epigenetically informed precision medicine in TBI.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by hallmark pathophysiological features, including the accumulation of amyloid-β (Aβ) plaques, hyperphosphorylation of Tau protein, synaptic degeneration, neuronal loss, and glial cell activation. Despite significant advances in research, the therapeutic options available remain limited, underscoring the necessity for the identification of novel therapeutic targets. Emerging evidence suggests a disruption of lipid metabolism in AD, with growing indications of a strong association between genes involved in lipid-related processes and the disease. This review aims to explore the role of lipid metabolism in AD, focusing on its impact on key pathological processes, including the deposition and clearance of Aβ, the seeding and propagation of Tau pathology, synaptic formation and function, and neuroinflammation.

Dry eye disease (DED) is an eye condition that primarily affects up to 30% of adults aged 50 years and older, impacting visual function and quality of life. The prevalence of the condition increases with age. Common symptoms of dry eye include dry eyes, redness, a sensation of having a foreign object in the eye, eye pain, sensitivity to light, increased eye discharge, eye itching, and visual fatigue. In this paper, we systematically review the primary pathological mechanisms of dry eye, the impact of aging on dry eye, and current strategies for clinical treatment.

Alzheimer's disease (AD), a prevalent form of dementia in the elderly, is characterized by marked neurodegeneration and cognitive decline. Central to its pathology are Amyloid-beta plaques, neurofibrillary tangles, and neuroinflammation. This review delves into the pivotal role of microglia, the primary immune cells in the central nervous system, in AD's progression. We highlight recent discoveries revealing how abnormal microglial activity, influenced by mitochondrial dysfunction, contributes to AD development. Special attention is given to the bidirectional relationship between microglia and mitochondria, including the impact of metabolic disturbances and energy dysregulation on microglial function. Further, we explore the mechanisms underlying microglial activation and its consequences on neuronal health, including the interplay between inflammatory pathways and mitochondrial dynamics. Our comprehensive analysis underscores the significance of mitochondrial homeostasis in microglial functionality and its implications for AD progression, offering insights into potential therapeutic avenues targeting microglial mitochondria in AD.