Neurodegenerative diseases (NDDs), including Alzheimer’s Disease (AD), Parkinson’s Disease (PD), and Huntington’s Disease (HD), share pathologic mechanisms including oxidative stress, mitochondrial dysfunction, and protein aggregation. However, they differ in age of onset and clinical progression. Emerging evidence highlights primary cilia (PC) as a key regulator of neuronal aging and the progression of these diseases. Dysfunctional PC may impair key signaling pathways, such as Sonic Hedgehog (Shh) and Wnt, promote oxidative stress, mitochondrial damage, and epigenetic instability. PC may also influence intercellular communication by regulating the biogenesis of exosomes and modulating tunneling nanotube (TNT) formation, both of which propagate toxic proteins between neurons. Mechanistically, the regulation of ciliary length is disrupted in AD, which leads to ciliary dysfunction that interferes with signaling pathways and promotes the aggregation of amyloid-beta. This amyloid-beta is then propagated through TNTs and exosomes, spreading neuronal damage. In PD, the accumulation of alpha-synuclein (α-syn) also impairs cilia function, thereby compromising the cell’s response to oxidative stress. This results in the formation of abnormal TNTs and defective exosome-mediated clearance, ultimately contributing to neurodegeneration. Similarly, the mutant huntingtin protein aggregates within primary cilia in HD, morphologically disrupting them by obstructing intraflagellar transport. Damaged cilia are also associated with increased TNT formation and the exosomal release of toxic proteins, which leads to mitochondrial and epigenetic instability, ultimately promoting neuronal aging. Together, targeting ciliary function and its downstream regulation of TNTs and exosomes may provide a novel approach for slowing or halting disease progression across neurodegenerative diseases.

Binge-eating disorder (BED), defined as recurrent episodes of consuming large amounts of food in a short period of time while experiencing a loss of control, remains difficult to manage. Although several pharmacological options are available, they often provide limited long-term benefit and may cause adverse effects. Emerging evidence suggests that gut microbiota dysbiosis contributes to BED pathophysiology. Cytokine infiltration of the gut barrier ultimately causes neuroinflammation, highlighting the gut–brain axis as a potential therapeutic target. This systematic review and meta-analysis evaluated the effectiveness and safety of central nervous system-targeting pharmacotherapies and psychobiotics for BED. Cochrane Library, PubMed, and the Virtual Health Library were searched for randomized controlled trials published from January 2000 to January 2026. Eligible studies evaluated monotherapy with a central nervous system-acting drug or psychobiotics in clinically diagnosed BED populations. Twenty pharmacological trials (n = 2154) and five psychobiotic trials (n = 304) met the inclusion criteria. Risk of bias was assessed using the Cochrane RoB 2 tool, and pooled estimates were calculated using random-effects models. Pharmacological interventions showed a significant pooled effect versus placebo (Standard Mean Difference (SMD) = 0.307, 95% Confidence Interval (CI): 0.103–0.511, p = 0.003), although heterogeneity warrants cautious interpretation. Psychobiotics showed a moderate and significant effect (SMD = 0.680, 95% CI: 0.448–0.913; I² (heterogeneity index) = 0%) and no reported adverse events. Overall, our study implies that psychobiotics may be a safe and potentially effective adjunctive approach for BED, but larger, well-designed trials are needed.