Why does Parkinson's make you lose your sense of smell, and how early does it start?

Why do you lose your sense of smell, and how many years ahead does it happen?

Physical tissue damage and disrupted wiring inside the brain cause early smell loss. Autopsy work by neuropathologist Hawkes showed significant nerve cell loss in the anterior olfactory nucleus, a primary brain structure processing smell. In living patients, functional magnetic resonance imaging shows disrupted signalling connectivity across primary and secondary olfactory networks. Diffusion imaging, a method mapping microstructural damage, reveals this damage spreads beyond dedicated smell pathways into tracts like the uncinate and inferior fronto-occipital fasciculi.

Smell loss typically appears between 3 and 17 years before movement symptoms. A 2019 meta-analysis of 7 prospective human studies tracking 3,272 participants with hyposmia, a reduced ability to smell, recorded 176 incident Parkinson's diagnoses. People with hyposmia had a 3.84-fold higher risk of developing Parkinson's than those with normal smell. In one included study by Ross and colleagues, hyposmia predated clinical motor diagnosis by at least 4 years in men. In the Parkinson's Associated Risk Syndrome study, an enriched subgroup of 185 participants with hyposmia completed assessments, and 25 developed Parkinson's over an average of 6.3 years.

The exact timeline remains uncertain because long-term studies disagree. Subgroup analyses in the 2019 meta-analysis found that prospective studies tracking participants for 5 to 10 years showed low variability, whereas studies extending beyond 10 years showed substantial divergence in their findings. A 2021 meta-analysis of longitudinal studies by Janssen Daalen and colleagues reported that the link between smell loss and incident Parkinson's was strongest in cohorts with shorter follow-up windows, weakening as the time between smell testing and diagnosis grew longer.

Why does the damage appear in the olfactory system before the movement centres?

Abnormal protein clumps accumulate in the smell pathways at the very earliest stage of the disease. Under Braak staging, a classification system tracking how pathology spreads through six sequential stages, abnormal protein aggregates called Lewy pathology, the characteristic protein clumps of the disease, appear in the olfactory bulb during Stage 1. An autopsy study of people with Parkinson's by Hawkes and colleagues revealed significant cell loss in the anterior olfactory nucleus, showing early protein buildup is accompanied by physical damage. Additionally, a 2016 meta-analysis of 6 case-control studies involving 216 patients and 175 controls found that the volume of the olfactory bulb was significantly reduced on both sides in those with the disease.

Where this damage actually originates remains unresolved. Under the dual-hit hypothesis, environmental pathogens enter the body through both the nose and the gut, triggering abnormal protein folding in both sites simultaneously. However, a newer body-first versus brain-first framework, which is a model proposing that Parkinson's has two different starting points, suggests that the nose is not always the source.

The disease may follow entirely separate pathways in different groups of patients. In the body-first subtype, pathology starts in the enteric nervous system, the web of nerves governing the gut, and travels up the vagus nerve, meaning the olfactory bulb is rarely involved early on. Conversely, in the brain-first subtype, the disease begins inside the central system itself, spreading through the olfactory bulb down to the substantia nigra, the brain region primarily responsible for producing dopamine. A small study using a seed amplification assay, a laboratory test that detects tiny quantities of misfolded protein, tested samples from skin biopsies and the nasal cavity to support these two distinct routes of spread.

Does your sense of smell keep worsening as your other symptoms progress?

Your sense of smell does not keep worsening once you receive a Parkinson's diagnosis. The loss of smell appears to occur early and then remain stable, showing no meaningful relationship with how long someone has had the disease or how severe their movement symptoms have become. This indicates that olfactory function plateaus rather than declining in tandem with ongoing clinical deterioration.

Large-scale reviews of existing studies show that disease duration does not affect smell test results. A 2021 meta-analysis of 125 cross-sectional studies, which evaluate different groups of people at a single point in time, analysed data from 6,593 individuals with Parkinson's and 8,731 healthy controls. When the researchers grouped these participants by how many years they had lived with the disease, they found no significant differences in smell test performance. Similarly, a 2018 systematic review of 27 studies concluded that odour identification tests deliver results independent of both disease duration and motor severity.

Comparing distinct groups of patients confirms that smell loss plateaus. A 2016 study compared patients from the Tracking Parkinson's cohort and the Oxford Discovery cohort, where 837 patients took a 16-item odour identification test. The patients in the Oxford Discovery group had lived with the disease longer and had worse motor severity. Despite these differences, there was no statistical evidence of a difference in their smell test scores, yielding a non-significant probability value of 0.12.

Does everyone with Parkinson's lose their sense of smell?

Between 10 per cent and 20 per cent of people with idiopathic Parkinson's keep a normal sense of smell. A meta-analysis of 23 studies involving 1,957 patients with Parkinson's disease showed that the sensitivity of olfactory testing to identify the disease was 79 per cent, meaning about 20 per cent of patients retain normal function. Another systematic review and meta-analysis of the olfactory bulb, the brain structure that processes smells, placed the overall prevalence of olfactory impairment in Parkinson’s at nearly 90 per cent.

The preservation of smell in certain genetic subtypes depends on where abnormal proteins accumulate. Patients carrying mutations in the GBA, LRRK2, or SNCA genes typically display peripheral synucleinopathy, where abnormal deposits of alpha-synuclein protein gather in nerves outside the brain and spinal cord. In contrast, patients carrying mutations in the PRKN gene do not have peripheral synucleinopathy, and they mostly lack these alpha-synuclein protein deposits in the brain entirely. While GBA, LRRK2, and SNCA variants are associated with lysosomal dysfunction, which impairs the cellular system for clearing waste, the PRKN variant is directly involved in mitochondrial dysfunction, which impairs cellular energy production.

Even within genetic subtypes, olfactory preservation is linked to a milder disease course. A study of 162 patients with the LRRK2 G2019S mutation used a 40-odorant identification test to categorise carriers by their smell performance. The researchers found that patients in the worst-performing smell category had an earlier age of disease onset and more rapid motor progression. Much of our understanding of these genetic cohorts comes from self-reported online surveys, such as a study of 6,883 patients from a genetic database, which are less precise than in-person clinical exams.

If you lose your sense of smell, how likely are you to develop Parkinson's?

Long-term screening studies show that roughly 13.5 per cent of older adults with objective hyposmia eventually develop Parkinson's. In the Parkinson Associated Risk Syndrome study, researchers tracked 185 participants who had unexplained hyposmia, defined as scoring at or below the 15th percentile on a smell identification test. Over an average follow-up of 6.3 years, 25 of these 185 individuals converted to Parkinson's disease, and one converted to dementia with Lewy bodies. This represents a total conversion rate to clinically diagnosable disease of 14 per cent.

These conversion rates are weakened by substantial selection bias. Although nearly 5,000 participants completed the standardized 40-odour scratch-and-sniff smell test, only 669 were found to have hyposmia. Of these, only 185 completed at least one follow-up visit, meaning 484 of the original hyposmic individuals did not participate in the longitudinal tracking. Furthermore, large-scale evidence remains incomplete, as the ongoing Parkinson's Progression Markers Initiative is collecting longitudinal follow-up data on an enriched subgroup of only 26 participants with hyposmia.

Objective testing is required because older adults cannot reliably self-report smell loss. In combined cohorts of 9,396 individuals, among those whose objective smell test fell at or below the 10th percentile, only 43 per cent of women and 52 per cent of men actually self-reported having a decreased sense of smell. This mismatch means that screening programmes cannot rely on simple questionnaires to identify at-risk individuals, restricting the feasibility of executing larger, long-term screening studies.

What this does not show

Predicting Parkinson's using smell loss is not unequivocally supported. A meta-analysis of seven prospective studies following 3,272 people with hyposmia and 176 Parkinson's cases concluded that smell loss is not a solid predictor of the disease. This symptom has low specificity because many other conditions can cause a reduced sense of smell.

Smell tests alone cannot reliably separate Parkinson's from other neurological mimics. A 2026 meta-analysis of 23 studies involving 1,957 patients with Parkinson's and 462 with atypical parkinsonian disorders found that smell tests alone are insufficient for a definite diagnosis. Most of the 23 studies carried a high risk of bias: they lacked random patient selection, performed tests under unblinded conditions, and adjusted scoring thresholds after collecting data to maximize accuracy.

Physical changes on brain scans are not consistently supported. A meta-analysis of six case-control studies involving 216 patients with Parkinson's and 175 healthy controls revealed contradictory results for olfactory bulb volume, with some studies showing no difference or even larger bulbs in patients. Similarly, a systematic review examining 15 diffusion MRI studies and 18 functional MRI studies of the olfactory pathways found a disconnect between visible structural damage in olfactory brain regions and the early functional loss of smell that patients report.

Finally, a new trial studying nasal biomarkers has not yet reported. A clinical trial registered as NCT07480187 is currently a trial registration attempting to build a molecular profile of Parkinson's disease using biomarkers in the olfactory mucosa. Because this study is currently a trial registration, it has not yet reported any results.

This evidence provides you with a clear map of why smell changes happen early in Parkinson's and how they stabilize over time. You can use these facts to discuss with your specialist whether an objective smell assessment is relevant to your specific symptoms, rather than relying on self-testing or guessing.