Author: Medical Team
Medical Blog
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The World Health Organization (WHO) estimates that there are 47.5 million dementia sufferers worldwide and that 7.7 million new cases are diagnosed each year. Frontotemporal dementia (FTD) disorders are responsible for 25% of dementia cases in people older than 65 years old, making them the second most common cause of dementia in patients under the age of 65 years.
Recent a study was published in “Annals of Clinical and Translational Neurology”, highlighting the role of different blood biomarkers in the early detection of FTD. Diagnosis of FTD is challenging due to the symptomatic overlap, neurodegeneration, heterogeneity of clinical presentation with other neurodegenerative diseases. PlGF, a novel blood biomarker is identified in the early detection of FTD
The early identification of FTD can be aided by particular blood biomarkers and neuroimaging, which are proving to be crucial biomarker clues. A growing body of research shows that Placental Growth Factor (PlGF) has biological impacts on pathological inflammation and angiogenesis linked to hematologic disorders, ischemia and cancer, in addition to its regulatory role during pregnancy. For the early identification of FTD, modulation of PlGF is also required in diseases associated with the central nervous system.
About Placental Growth Factor (PlGF)
Frontotemporal dementia (FTD) is one of the most common early-onset dementia with a reported prevalence rate of 3–26% in demented people with disease onset before 65 years of age.
A vascular endothelial growth factor (VEGF) family member, PlGF was first identified in the placenta but was later discovered to be expressed in other tissues. Elevated cerebrospinal fluid (CSF) levels of PlGF in Parkinson’s disease (PD), Parkinson’s disease dementia (PDD) and dementia with lewy bodies (DLB) has been investigated.
About the Study
At the Memory Clinic of Skane University Hospital in Malmo, Sweden, 75 patients with Alzheimer's disease (AD), 47 patients with Dementia with Lewy Bodies and Parkinson Disease (DLB-PDD), 33 patients with vascular dementia (VaD), 27 patients with FTD, and 50 healthy controls were enrolled in the cohort study.
In this cohort study, 96 people (recruited from the same clinic) had a baseline diagnosis of mild cognitive impairment (MCI). 34 of those had converted to AD (MCI-AD) after an average clinical follow-up duration of 5.7 years (3.0-9.6), whereas 62 had retained cognitive stability (sMCI). Medical professionals with considerable experience in cognitive problems evaluated each trial participant.
Higher accuracies for PlGF were found in a sub-cohort analysis (n=267) that compared the diagnostic performance of PlGF alone, with tau, and with tau and amyloid-beta 42 to neurofilament light chain. In all the subjects CSF levels of PlGF were analysed.
CSF sampling and biological assays
CSF samples were taken from all patient groups and control groups that weren't fasting. To prevent gradient effects, CSF was collected in polypropylene tubes and carefully mixed. To remove cells and debris, all samples were centrifuged within 30 minutes at +4°C at 2000g for 10 min. In anticipation of biochemical examination, samples were kept in aliquots at 80°C. Using electrochemiluminescence immunoassay, CSF PLGF was quantified.
|
Control (n = 50) |
sMCI (n = 62) |
MCI – AD (n = 34) |
AD (n = 75) |
DLB – PDD (n = 47) |
VaD (n = 33) |
FTD (n = 27) |
Age |
74.2 |
69.2 |
74.9 |
76.4 |
74.5 |
75.9 |
70.1 |
Sex, (% Female) |
72% |
56% |
65% |
68% |
40% |
46% |
44% |
Apolipoprotein E (APOE) |
27% |
47% |
82% |
65% |
54% |
25% |
27% |
Mini‐Mental State Examination (MMSE) |
29.0 |
28.2 |
26.4 |
19.5 |
21.9 |
21.7 |
22.8 |
Aβ42, pg/ml |
695 |
486 |
317 |
260 |
340 |
396 |
709 |
Aβ40, pg/ml |
5206 |
3821 |
4232 |
3899 |
3170 |
3238 |
4509 |
tau, pg/ml |
443 |
437 |
645 |
766 |
472 |
441 |
385 |
PlGF, pg/ml |
54.8 |
64.1 |
70.5 |
79.5 |
89.5 |
94.2 |
166.7 |
Table 1.1 CSF levels of PlGF in Diagnostic Groups
Conclusion
The findings imply that PlGF presents a very promising biomarker for the early identification of FTD. Individuals with FTD have concentrations that are 1.8–2.1 times greater than those of people with AD, DLB–PDD, and VaD. By separating FTD from both controls and sMCI, PlGF alone displayed extremely high accuracies, sensitivities, and specificities.
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