scholarly journals Butyrylcholinesterase K variant is genetically associated with late onset Alzheimer's disease in Northern Ireland

2000 ◽  
Vol 37 (3) ◽  
pp. 182-185 ◽  
Author(s):  
S P McIlroy
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Northern Ireland ◽  
Late Onset ◽  
K Variant

Association of butyrylcholinesterase K variant with cholinesterase-positive neuritic plaques in the temporal cortex in late-onset Alzheimer's disease

2000 ◽  
Vol 106 (4) ◽  
pp. 447-452 ◽  
Author(s):  
Donald J. Lehmann ◽  
Zsuzsanna Nagy ◽  
Suzanne Litchfield ◽  
Mario Cortina Borja ◽  
A. David Smith
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Temporal Cortex ◽  
Neuritic Plaques ◽  
K Variant

scholarly journals Butyrylcholinesterase Protein Ends in the Pathogenesis of Alzheimer’s Disease—Could BCHE Genotyping Be Helpful in Alzheimer’s Therapy?

Biomolecules ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 592 ◽  
Author(s):  
Jacek Jasiecki ◽  
Bartosz Wasąg
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
At Risk ◽  
Enzyme Activity ◽  
Late Onset ◽  
Past Century ◽  
Nucleotide Polymorphisms ◽  
Amino Acid Residues ◽  
Patients At Risk ◽  
K Variant

Late-onset Alzheimer’s disease (AD) is clinically characterized by a progressive decline of memory and other cognitive functions leading to the loss of the ability to perform everyday activities. Only a few drugs have been approved to treat AD dementia over the past century since the first AD patient was diagnosed. Drugs increasing the availability of neurotransmitters at synapses in the brain are used clinically in the treatment of AD dementia, and cholinesterase inhibitors (ChEIs) are the mainstay of the therapy. A detrimental effect on cognitive function has been reported in patients with pharmacological inhibition of acetylcholinesterase (AChE) by ChEIs and reduced butyrylcholinesterase (BChE) activity due to the single nucleotide polymorphisms. The BChE K-variant (rs1803274), the most common genetic variant of the BCHE gene, was thought to reduce enzyme activity reflecting the lower clinical response to rivastigmine in AD patients. During ChEIs therapy, patients carrying reduced-activity BChE do not present such improved attention like patients with the wild-type enzyme. On the other hand, alterations in the BCHE gene causing enzyme activity reduction may delay AD onset in patients at risk by preserving the level of cortical acetylcholine (ACh). Based on our previous results, we conclude that SNPs localized outside of the coding sequence, in 5’UTR (rs1126680) and/or intron 2 (rs55781031) of the BCHE gene, but not solely K-variant alteration (p.A539T) itself, are responsible for reduced enzyme activity. Therefore, we suspect that not BChE-K itself, but these coexisting SNPs (rs1126680 and rs55781031), could be associated with deleterious changes in cognitive decline in patients treated with ChEIs. Based on the results, we suggest that SNPs (rs1126680) and/or (rs55781031) genotyping should be performed to identify subjects at risk for lowered efficacy ChEIs therapy, and such patients should be treated with a lower rivastigmine dosage. Finally, our sequence analysis of the N-terminal end of N-BChE revealed evolutionarily conserved amino acid residues that can be involved in disulfide bond formation and anchoring of N-BChE in the cell membrane.

K variant of butyrycholinesterase and late-onset Alzheimer's disease

The Lancet ◽  
1998 ◽  
Vol 351 (9106) ◽  
pp. 881 ◽  
Author(s):  
C Russ ◽  
J Powell ◽  
S Lovestone ◽  
C Holmes
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
K Variant

scholarly journals Synergy between the alteration in the N-terminal region of butyrylcholinesterase K variant and apolipoprotein E4 in late-onset Alzheimer’s disease

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jacek Jasiecki ◽  
Anna Limon-Sztencel ◽  
Monika Żuk ◽  
Magdalena Chmara ◽  
Dominik Cysewski ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Terminal Region ◽  
Apolipoprotein E4 ◽  
K Variant

Butyrylcholinesterase K variant and apolipoprotein E4 genes do not act in synergy in Finnish late-onset Alzheimer's disease patients

1998 ◽  
Vol 250 (1) ◽  
pp. 69-71 ◽  
Author(s):  
Mikko Hiltunen ◽  
Arto Mannermaa ◽  
Seppo Helisalmi ◽  
Anne Koivisto ◽  
Maarit Lehtovirta ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Apolipoprotein E4 ◽  
K Variant

Familial Patterns of Risk in Very Late-Onset Alzheimer's Disease

2003 ◽  
Author(s):  
J. M. Silverman ◽  
C. J. Smith ◽  
D. B. Marin ◽  
R. C. Mohs ◽  
C. B. Propper
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Familial Patterns
Sign in / Sign up

Export Citation Format

Share Document