Immuno-Diagnostics Antibodies and Antigens for Parkinson's Disease (PD)


What is Parkinson's Disease (PD)?

Parkinson's disease is a neurodegenerative disorder that primarily affects the motor system. Such a loss of dopamine producing neurons in the substantia nigra region of the brain causes the disease, which results in less dopamine. Dopamine is as important a neurotransmitter as it is to the movement as it is to the emotional responses. These neurons are damaged or killed leading to the characteristic motor and non-motor symptoms seen in Parkinson's disease [1-2].

Pathological Changes in Parkinson's Disease

1. Loss of Dopamine Neurons: Parkinson’s disease is primarily characterized simply by the progressive loss of dopamine-releasing neurons in substantia nigra, a movement control locale of the brain. This loss causes a decrease in dopamine in the brain; decreased brain signaling and production of dopamine leads to motor signs such as tremors, rigidity, and bradykinesia .

2. Formation of Lewy Bodies: The other pathological hallmark is the presence of proteinaceous cytoplasmic inclusion bodies called Lewy bodies inside neurons. These deposits by and large contain α-synuclein protein and interfere with cell physiology thus leading to neuronal death. Originally thought to be observed only in SN, LB are also present in other regions of the brain, which can cause a number of nonmotor symptoms, such as cognitive impairment and mood changes.

3. Neurotransmitter Changes: In addition to dopamine, Parkinson’s disease involves a reduction of serotonin, norepinephrine, and acetylcholine neurotransmitters. All these changes cause the non motor manifestations such as depression, sleep wake syndrome and autonomic dysfunction.

All these pathological changes collectively explain the motor-symptom saturated view of parkinsonism and the necessity for combined motor and non-motor symptom pharmacological management.

Diagnosis of Parkinson's Disease

Parkinson’s disease requires careful diagnosis to diagnose the condition correctly and to rule out other conditions with similar symptoms. Clinical symptom assessment is centered on the documentation of traditional motor abnormality signs such as tremor, rigidity, and akinesia. A neurological examination tests reflexes and coordination, muscle strength, and tone. The drug response test measures the improvement after giving dopaminergic treatments; common a PD symptom. MRI for instance or DaT scan precludes other conditions and evaluates the dopamine transporter. The use of novel biomarker tests such as alpha synuclein, DJ-1, and Neurofilament light chain (NfL) gives relevant information about the diseases anatomic distribution and evolution. This way, integration of these methods provides accurate and comprehensive diagnosis of Parkinson’s disease.

Humain Brain PNG, Vector And Transparent Clipart Images

Figure 1. Source: Humain Brain PNG, Vector And Transparent Clipart Images




Validation data


  • Aβ40/Aβ42

Good performance of GeneMedi's Aβ40/Aβ42 antibodies in ELISA and CLIA Validation

The high-performance Aβ40 and Aβ42 antibody raw materials developed by GeneMedi have the advantages of good specificity and high sensitivity, and are the preferred raw materials for the development of in vitro diagnostics reagents for Alzheimer's disease.
In direct ELISA analysis, GMP-h-Aβ40-Ab01 and GMP-h-Aβ42-Ab01 can Recognizes Aβ40 or Aβ42 with high specificity. GMP-h-Aβ42-Ab02 has cross-reactivity with both Aβ40 and Aβ42.
In CLIA verification, the antibody pair (Capture: GMP-h-Aβ40-Ab01 , Detect: GMP-h-Aβ42-Ab02 ) can detect the GMP-h-Aβ40-Ag01, and the antibody pair (Capture: GMP-h-Aβ42-Ab02 , Detect: GMP-h-Aβ42-Ab01 ) can detect the GMP-h-Aβ42-Ag01. Beta-amyloid(1-42) antibodies (GMP-h-Aβ42-Ab02 and GMP-h-Aβ42-Ab01) established a standard curve, and the detection range of Aβ42 was 100-1700 pg/mL.

Figure 1: Good performance of GeneMedi's Aβ40/Aβ42 antibodies in ELISA and CLIA Validation

A. GMP-h-Aβ40-Ab01 and GMP-h-Aβ42-Ab02 can bind GMP-h-Aβ40-Ag01, while GMP-h-Aβ42-Ab01 can not bind the Aβ40 antigen in direct ELISA.
B. GMP-h-Aβ42-Ab01 and GMP-h-Aβ42-Ab02 can bind GMP-h-Aβ42-Ag01, while GMP-h-Aβ40-Ab01 can not bind the Aβ42 antigen in direct ELISA.
C. CLIA verification data of the antibody pair (Capture: GMP-h-Aβ40-Ab01 , Detect: GMP-h-Aβ42-Ab02 ) to detect the GMP-h-Aβ40-Ag01.
D. CLIA verification data of the antibody pair (Capture: GMP-h-Aβ42-Ab02 , Detect: GMP-h-Aβ42-Ab01 ) to detect the GMP-h-Aβ42-Ag01.

Aβ42 validation

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Biomarkers for Parkinson's Disease



Table 1. Key biomarkers in blood and their detection limits
Biomarker Limit (Pathological concentration in blood)
Human Parkinsonism associated deglycase (PARK7) /
Alpha-synuclein (α-synuclein) >10 pg/ml
Tau proteins (Tau) >10 pg/ml
Neurofilament light chain (NfL) /
Glial fibrillary acid protein (GFAP) /
Beta-amyloid 42 (Aβ42) /
Beta-amyloid 40 (Aβ40) >100 pg/ml

Sample Types: Blood, cerebrospinal fluid (CSF)



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