Intranasal administration is widely presented as a route that circumvents the blood-brain barrier and delivers therapeutics directly to the degenerating brain. Three decades of preclinical work support the existence of olfactory, trigeminal and perivascular pathways from the nasal mucosa to the central nervous system, yet no product is approved for a neurodegenerative indication on the strength of direct nose-to-brain transport, and the largest completed trial in the field returned a null result confounded by a mid-study change of delivery device. This review appraises that gap. The mechanistic case for the route is examined against the anatomical evidence, and the quantitative preclinical literature is evaluated on its own terms. Reported drug targeting efficiency values for broadly comparable rodent intranasal studies span roughly 158% to 2362%, a spread that is not explained by the physicochemical properties of the compounds involved, and a standardised rat screening programme found blood and tissue ratios to be highly variable and not always reproducible. Systematic quantitative analysis of the published record indicates that particulate and gel-based carriers confer limited advantage over simple drug solution. Against this, human data are sparse but instructive: intranasal glutathione raised brain glutathione measured by magnetic resonance spectroscopy yet failed to outperform placebo in a randomised phase IIb trial, and intranasal oxytocin raised cerebrospinal fluid concentrations on a time course dissociated from plasma. The argument advanced is that the binding constraint on translation is evidentiary rather than technological. The field reports a metric it cannot standardise, in species whose nasal anatomy does not scale, using devices that have no clinical counterpart. A route-specific reporting standard is proposed as an extension of ARRIVE 2.0, covering dose placement, administration volume, anaesthetic state, systemic controls, analytical validation, absolute delivered fraction and device disclosure.