Onset age of Parkinson disease

Inzelberg, Rivka; Schechtman, Edna; Paleacu, Diana

doi:10.1002/ajmg.10586

Cited by 15 publications

(10 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inzelberg et al [2002] confirm our finding of earlier onset in patients with positive family history. They further suggest that earlier onset in ε4 carriers may be due to family history and patients with parkin mutations.…”

Section: To the Editorsupporting

confidence: 88%

“…In a study of 521 unrelated Caucasian PD patients, we found that ε3ε4/ε4ε4 patients had significantly earlier onset than ε3ε3 patients [Zareparsi et al, 2002]. Inzelberg et al [2002] have combined the samples from different studies and report that they do not detect a significant difference in onset among ε4 carriers and those without ε4.…”

Section: To the Editormentioning

confidence: 99%

See 1 more Smart Citation

Reply to correspondence from Inzelberg et al.—“onset age of Parkinson disease”

Zareparsi

Payami

2002

Am. J. Med. Genet.

View full text Add to dashboard Cite

Section: To the Editorsupporting

confidence: 88%

Section: To the Editormentioning

confidence: 99%

Reply to correspondence from Inzelberg et al.—“onset age of Parkinson disease”

Zareparsi

Payami

2002

Am. J. Med. Genet.

View full text Add to dashboard Cite

“…Parkinson disease (PD) is a progressive neurodegenerative disorder, characterized by loss of dopaminergic neurons in the substantia nigra. Although the median age at onset is 60 years, 30 to 50% loss of substantia nigra dopaminergic neurons may occur before the clinical diagnosis of PD . Thus, there may be a window for intervention to slow or halt disease progression, after the onset of pathophysiology, but prior to the development of manifest clinical disease, if high‐risk individuals could be identified.…”

mentioning

confidence: 99%

Plasma apolipoprotein A1 as a biomarker for Parkinson disease

Qiang

Wong

Siderowf³

et al. 2013

Annals of Neurology

123

109

View full text Add to dashboard Cite

Objective To identify plasma-based biomarkers for Parkinson's Disease (PD) risk. Methods In a discovery cohort of 152 PD patients, plasma levels of 96 proteins were measured by multiplex immunoassay; proteins associated with age at PD onset were identified by linear regression. Findings from discovery screening were then assessed in a second cohort of 187 PD patients, using a different technique. Finally, in a third cohort of at-risk, asymptomatic individuals enrolled in the Parkinson's Associated Risk Study (PARS, n=134), plasma levels of the top candidate biomarker were measured, and dopamine transporter (DAT) imaging performed, to evaluate the association of plasma protein levels with dopaminergic system integrity. Results One of the best candidate protein biomarkers to emerge from discovery screening was apolipoprotein A1 (ApoA1, p=0.001). Low levels of ApoA1 correlated with earlier PD onset, with a 26% decrease in risk of developing PD associated with each tertile increase in ApoA1 (Cox proportional hazards p<0.001, hazard ratio=0.742). The association between plasma ApoA1 levels and age at PD onset replicated in an independent cohort of PD patients (p<0.001). Finally, in the PARS cohort of high-risk, asymptomatic subjects, lower plasma levels of ApoA1 were associated with greater putaminal DAT deficit (p=0.037). Interpretation Lower ApoA1 levels correlate with dopaminergic system vulnerability in symptomatic PD patients and in asymptomatic individuals with physiological reductions in dopamine transporter density consistent with prodromal PD. Plasma ApoA1 may be a new biomarker for PD risk.

show abstract

“…PD not only shortens the life expectancy but also causes debility during life affecting quality of life [278]. Mean age of onset of PD was estimated to be in the late 50s [111], however now it is thought to be in the early-to-mid 60s [121]. In 5-10% of the patients initial symptoms arise between age 10 and 40 (sometimes 50) years, hence is termed as young onset PD [85].…”

Section: Epidemiologymentioning

confidence: 98%

Parkinsons Disease: Genetics and Beyond

Inamdar

Arulmozhi

Tandon³

et al. 2007

View full text Add to dashboard Cite

Parkinson's disease (PD) is characterized clinically by resting tremor, rigidity, bradykinesia and postural instability due to progressive and selective loss of dopamine neurons in the ventral substantia nigra, with the presence of ubiquitinated protein deposits called Lewy bodies in the neurons. The pathoetiology of cell death in PD is incompletely understood and evidence implicates impaired mitochondrial complex I function, altered intracellular redox state, activation of proapoptotic factors and dysfunction of ubiquitinproteasome pathway. Now it is believed that genetic aberration, an environmental toxin or combination of both leads to a cascade of events culminating in the destruction of myelinated brainstem catecholaminergic neurons. Also the role of production of significant levels of abnormal proteins, which may misfold, aggregate and interfere with intracellular processes causing cytotoxicity has recently been hypothesized. In this article, the diverse pieces of evidence that have linked the various factors responsible for the pathophysiology of PD are reviewed with special emphasis to various candidate genes and proteins. Furthermore, the present therapeutic strategies and futuristic approaches for the pharmacotherapy of PD are critically discussed.

show abstract

Onset age of Parkinson disease

Cited by 15 publications

References 8 publications

Reply to correspondence from Inzelberg et al.—“onset age of Parkinson disease”

Reply to correspondence from Inzelberg et al.—“onset age of Parkinson disease”

Plasma apolipoprotein A1 as a biomarker for Parkinson disease

Parkinsons Disease: Genetics and Beyond

Contact Info

Product

Resources

About