Parkinson's disease (PD) is a common neurodegenerative disorder with a lifetime incidence of approximately 2 percent. A pattern of familial aggregation has been documented for the disorder, and it was recently reported that a PD susceptibility gene in a large Italian kindred is located on the long arm of human chromosome 4. A mutation was identified in the α-synuclein gene, which codes for a presynaptic protein thought to be involved in neuronal plasticity, in the Italian kindred and in three unrelated families of Greek origin with autosomal dominant inheritance for the PD phenotype. This finding of a specific molecular alteration associated with PD will facilitate the detailed understanding of the pathophysiology of the disorder.

/pdf/mutation-in-the-a-synuclein-gene-identified-in-families-with-17me93ny5f.pdf

Mutation in the α-synuclein gene identified in families with Parkinson's disease

Olfactory dysfunction is among the earliest nonmotor features of Parkinson disease (PD). Such dysfunction is present in approximately 90% of early-stage PD cases and can precede the onset of motor symptoms by years. The mechanisms responsible for olfactory dysfunction are currently unknown. As equivalent deficits are observed in Alzheimer disease, Down syndrome, and the Parkinson-dementia complex of Guam, a common pathological substrate may be involved. Given that olfactory loss occurs to a lesser extent or is absent in disorders such as multiple system atrophy, corticobasal degeneration, and progressive supranuclear palsy, olfactory testing can be useful in differential diagnosis. The olfactory dysfunction in PD and a number of related diseases with smell loss correlates with decreased numbers of neurons in structures such as the locus coeruleus, the raphe nuclei, and the nucleus basalis of Meynart. These neuroanatomical findings, together with evidence for involvement of the autonomic nervous system in numerous PD-related symptoms, suggest that deficits in cholinergic, noradrenergic and serotonergic function may contribute to the olfactory loss. This Review discusses the current understanding of olfactory dysfunction in PD, including factors that may be related to its cause.

Olfactory dysfunction in Parkinson disease

Background Olfactory deficits in Alzheimer's disease (AD) and idiopathic Parkinson's disease (PD) have been well established. Objective To clarify and review the literature by evaluating the evidence for olfactory deficits in 3 olfactory domains, including odor identification, recognition, and detection threshold. Data Sources A literature search of English-language studies of olfaction in AD, PD, and healthy controls was conducted via online databases (PsycInfo and MEDLINE) and reference lists from review articles. Study Selection To meet selection criteria for meta-analysis, each study required a control group and complete and usable data. This review yielded 26 publications of olfactory identification, recognition, and/or detection threshold. Because of the inclusion of more than 1 relevant study of olfaction in several of these publications (eg, both identification and threshold assessed), 43 studies were ultimately appropriate for meta-analysis. Data Extraction Effect sizes were calculated for each study by expressing differences between patient and control group means in SD units (Cohen's d ). Data Synthesis Extremely large effect sizes were shown across all tasks in both AD and PD groups. Both between-group analyses using the Mann-Whitney U test and within-group analyses using Friedman 2-way analysis of variance did not reveal any significant differences (all P >.30). Conclusions As expected, severe deficits were found for both patients with AD and PD in each of the 3 olfactory domains relative to controls. However, no discriminating olfactory deficits were seen between patient groups or among the 3 measured olfactory domains, suggesting a similar disturbance in olfactory function between patients with AD and PD.

https://jamanetwork.com/journals/jamaneurology/articlepdf/773547/noc7055.pdf

Olfaction in Neurodegenerative Disease: A Meta-analysis of Olfactory Functioning in Alzheimer's and Parkinson's Diseases

Olfaction in Parkinson's disease and related disorders

Environmental agents, including viruses, prions, and toxins, have been implicated in the cause of a number of neurodegenerative diseases, most notably Alzheimer's and Parkinson's diseases. The presence of smell loss and the pathological involvement of the olfactory pathways in the formative stages of Alzheimer's and Parkinson's diseases, together with evidence that xenobiotics, some epidemiologically linked to these diseases, can readily enter the brain via the olfactory mucosa, have led to the hypothesis that Alzheimer's and Parkinson's diseases may be caused or catalyzed by agents that enter the brain via this route. Evidence for and against this concept, the "olfactory vector hypothesis," is addressed in this review.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1002/ana.21327

The olfactory vector hypothesis of neurodegenerative disease: is it viable?

The olfactory function of 6 patients whose parkinsonism was the result of intravenous administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was compared to that of 12 age-matched patients with idiopathic Parkinson's disease (PD) and 10 age-matched normal control subjects. Unlike their PD counterparts, the olfactory test scores of patients with MPTP-induced parkinsonism, did not differ significantly from those of control subjects. These findings suggest that MPTP induced parkinsonism, unlike idiopathic PD, is unaccompanied, on average, by major alterations in the ability to smell.

Lack of major olfactory dysfunction in MPTP-induced parkinsonism.

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Lack of major olfactory dysfunction in MPTP-induced parkinsonism.