Acetylcholinesterase and Butyrylcholinesterase of Developing Human Brain

Kaplay, Suresh S.

doi:10.1159/000240805

Cited by 32 publications

(17 citation statements)

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“…Gale did not provide CAT values on fetal or neonatal brains of more than 26 weeks GA (apart from one at 28 weeks) which would allow comparison with the older specimens in our series, but the downward trend of the values from 15-17 weeks, in both cerebral cortex and cerebellum, reported by Gale was not observed in our material. Our absolute values for AchE are broadly in accord with values reported for fetal brain [28,30]. Although our adult values for cere bral cortex, but not for cerebellum, are sub stantially lower than those recently published by MacKay et al [36], they are of the same order as those of other authors [6,16,35], who also report much lower AchE activity in cerebral cortex than in cerebellum.…”

Section: Discussionsupporting

confidence: 91%

“…Although the biochemical ontogenesis of neurotransmitter systems has been extensively studied in animals [for recent reviews see 10,33], data on this aspect of brain development in man has so far been very limited: histochemical studies of the development of rnonoaminergic neurones in fetal brain [see 10 and earlier work quoted therein]; preliminary data on choline acetyllransferase (CAT) activity in 5 fetal brains of 8-32 weeks gestational age (GA) [7]; a recent report [24] on the onto genesis of CAT and of glutamate decarboxy lase (GAD) in brains from 21 fetuses between 11 and 28 weeks GA; several early reports on fetal and infant brain acetylcholinesterase (AchE) [see review by Silver,40], amplified by a more systematic regional study [30]; studies of concentration changes with age of thyrotrophin-and luteinizing hormone-releas ing hormones in different regions [1,44]; re ported failure to find detectable concentra tions of tyrosine hydroxylase in 7 fetal brains [3],…”

Section: Introductionmentioning

confidence: 99%

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Biochemical Development of the Human Brain

Brooksbank¹,

Martínez²,

Atkinson³

et al. 1978

Dev Neurosci

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The development of the cholinergic system in the human forebrain, cerebral cortex and cerebellum was studied in post mortem material by estimating activity of choline acetyltransferase (CAT) and the binding capacity for quinuclidinyl benzilate (QNB) as markers for cholinergic nerve terminals and muscarinic receptors respectively; also the activity of acetylcholinesterase (AchE) was determined. The age periods were as follows (number of specimens in parentheses): fetal period, 18–22 weeks gestational age(GA; 8). perinatal period, 26–44 weeks GA (5–15 depending on brain part), early postnatal period, 2–15 months (4), and adult life, 58–70 years (4). Total protein and DNA were estimated in all specimens, and whole organ weights were obtained for the forebrain and most of the cerebellum specimens, allowing assessment of total organ parameters. Marked differences were observed in the ontogenesis of the cholinergic system in the cerebrum and the cerebellum. In the cerebral cortex and the forebrain from 18 weeks gestation towards term there was an increase in the concentration of CAT activity, which, however, had not reached adult concentrations at birth; on the other hand, receptor development was more advanced, since QNB binding site concentration reached adult levels by term. In sharp contrast, in the cerebellum maximal CAT activity was attained in the 26–42 weeks GA group. In comparison with the concentration of this presynaptic marker at that age period, the estimates in the postnatal samples were only 10–18%, the precipitous decline occurring during the early postnatal period. The highest concentration of the cholinergic ligand binding sites was also reached during gestation, but the peak was attained earlier (18–22 weeks GA) and the fall in concentration with age was less sharp. In contrast to the developmental changes in the concentration of the muscarinic receptor the affinity for the ligand was apparently the same throughout the age period studied. AchE activity in cerebral cortex increased with development to a level higher than that found in the adult, while the cerebellum was much richer in AchE and there was a modest developmental increase, the highest concentrations being found in adult cerebellum.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Biochemical Development of the Human Brain

Brooksbank¹,

Martínez²,

Atkinson³

et al. 1978

Dev Neurosci

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“…BChE is a nonspecific choline esterase, which is abundant in blood, liver, and brain 5. Altered serum BChE activity might indicate a disrupted Ach hydrolysis, which would, in turn, indirectly signal an imbalance between the pro- and anti-inflammatory systemic responses mediated by nonneuronal cholinergic activity 4,6.…”

Section: Introductionmentioning

confidence: 99%

Reduced butyrylcholinesterase activity is an early indicator of trauma-induced acute systemic inflammatory response

Zivkovic¹,

Bender²,

Brenner³

et al. 2016

JIR

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PurposeEarly diagnosis of systemic inflammatory response syndrome is fundamentally important for an effective and a goal-directed therapy. Various inflammation biomarkers have been used in clinical and experimental practice. However, a definitive diagnostic tool for an early detection of systemic inflammation remains to be identified. Acetylcholine (Ach) has been shown to play an important role in the inflammatory response. Serum cholinesterase (butyrylcholinesterase [BChE]) is the major Ach hydrolyzing enzyme in blood. The role of this enzyme during inflammation has not yet been fully understood. This study tests whether a reduction in the BChE activity could indicate the onset of the systemic inflammatory response upon traumatic injury.Patients and methodsThis observational study measured BChE activity in patients with traumatic injury admitted to the emergency room by using point-of-care-test system (POCT). In addition, the levels of routine inflammation biomarkers during the initial treatment period were measured. Injury Severity Score was used to assess the trauma severity.ResultsAltered BChE activity was correlated with trauma severity, resulting in systemic inflammation. Reduction in the BChE activity was detected significantly earlier compared to those of routinely measured inflammatory biomarkers.ConclusionThis study suggests that the BChE activity reduction might serve as an early indicator of acute systemic inflammation. Furthermore, BChE activity, measured using a POCT system, might play an important role in the early diagnosis of the trauma-induced systemic inflammation.

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“…On the other hand, the enzyme butyrylcholin-esterase (BuChE) (also known as “pseudo” cholinesterase; EC 3.1.1.8) is a non-specific type of cholinesterase enzyme that hydrolyzes different types of choline esters and it ubiquitously exists throughout the body, most importantly, in the human liver, blood serum, pancreas and the central nervous system. In the brain, BuChE is primarily associated with glial cells and endothelial cells [1, 2]. …”

Section: Introductionmentioning

confidence: 99%

Status of Acetylcholinesterase and Butyrylcholinesterase in Alzheimer's Disease and Type 2 Diabetes Mellitus

Mushtaq¹,

Greig²,

Khan³

et al. 2014

CNSNDDT

262

175

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Both Alzheimer’s disease (AD) and Type 2 diabetes mellitus (T2DM) share the presence of systemic and neuro-inflammation, enhanced production and accumulation of β-amyloid peptide and abnormal levels of the enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). Altered levels of AChE and BuChE both in AD as well as in T2DM imply that those two enzymes may be playing a pivotal role in the pathogenesis of the two disorders. AD and T2DM are both characterized by elevated levels of AChE and BuChE in the plasma. On the other hand, in AD the brain levels of AChE go down while those of BuChE go up, resulting in deregulation in balance between AChE and BuChE. This imbalance and change in the AChE/BuChE ratio causes cholinergic deficit in the brain, i.e. deficiency in the brain neurotransmitter acetylcholine. With better understanding of the inter-relationship of AChE and BuChE levels in normality as well as abnormality, AD and T2DM can be effectively treated. Thus, general cholinesterase inhibitors that inhibit both AChE and BuChE as well as highly selective BuChE inhibitors may have potential therapeutic benefits in the treatment of AD and other related dementias.

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Acetylcholinesterase and Butyrylcholinesterase of Developing Human Brain

Cited by 32 publications

References 2 publications

Biochemical Development of the Human Brain

Biochemical Development of the Human Brain

Reduced butyrylcholinesterase activity is an early indicator of trauma-induced acute systemic inflammatory response

Status of Acetylcholinesterase and Butyrylcholinesterase in Alzheimer's Disease and Type 2 Diabetes Mellitus

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Acetylcholinesterase and Butyrylcholinesterase of Developing Human Brain

Cited by 32 publications

References 2 publications

Biochemical Development of the Human Brain

Biochemical Development of the Human Brain

Reduced butyrylcholinesterase activity is an early indicator of trauma-induced acute systemic inflammatory response

Status of Acetylcholinesterase and Butyrylcholinesterase in Alzheimer&#39;s Disease and Type 2 Diabetes Mellitus

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Status of Acetylcholinesterase and Butyrylcholinesterase in Alzheimer's Disease and Type 2 Diabetes Mellitus