|
| Author(s), reference | Country | Population characteristics | Genes studied | Method of analysis | Summary findings | Study limitations |
|
| Okubadejo et al. [38] | Nigeria | PD cases: 57
Males: 43 (75.4%)
Females: 14 (24.6%)
Age at study [mean ± SD (range)]: 62.3 ± 9.1 (43–80) y | ATXN3
LRRK2
PRKN | Screen for pathogenic repeat expansions
Sanger sequencing of exons 31 and 41
Sanger sequencing of all exons and exon/intron boundaries | No pathogenic expansions
No variants
Several variants but none pathogenic | Small sample size; thus, definite conclusions about the prevalence of gene mutations are unachievable. |
|
| Cilia et al. [25] | Ghana | PD cases: 54
Males: 33 (61.1%)
Females: 21 (75.4%)
Age at study [mean ± SD (range)]: 65 ± 12 (34–89) y
Age at onset [mean ± SD (range)]: 59.5 ± 12 (30–83) y | LRRK2 | Sequencing of exon 31 and exon 41 with their intron-exon boundaries | One nonpathogenic variant | Small sample size; thus, definite conclusions about the prevalence of gene mutations are unachievable. |
|
| Okubadejo et al. [18] | Nigeria | PD cases: 123
Males: 93 (73.8%)
Females: 3 (26.2%)
Age at study [mean ± SD (range)]: 61.9 ± 9.9 (36–81) y
Age at onset [mean ± SD]: 59.0 ± 13 y | LRRK2 | Kompetitive Allele Specific PCR (KASP) assay to screen for p.G2019S mutation | LRRK2 p.G2019S mutation is not implicated in PD in Nigerian patients | 1. Other known mutations of the LRRK2 gene were not screened.
2. Screening method did not allow for the identification of novel pathologic variants. |
|
| Rizig et al. [12] | Nigeria | PD cases: 92
Males: 70 (76.1%)
Females: 22 (23.9%)
Age at study [mean ± SD (range)]: 62.1 ± 9.2 (39–90) y
Age at onset [mean ± SD (range)]: 58.8 ± 9.4 (36–78) y | LRRK2 | Kompetitive Allele Specific PCR (KASP) assay of 12 variants | LRRK2 pathogenic alleles were absent for all 12 SNPs | 1. Other known mutations of the LRRK2 gene were not screened.
2. Screening method did not allow for the identification of novel pathologic variants. |
|
