Not exact matches
Specifically, intensive postmortem neurological studies
of their brain tissues reveal a relatively low density
of acetylcholine (a neurotransmitter) nerve sites, which, at normal densities,
function in critical ways to help re-initiate breathing following a sleep - related apnea or extended breathing pauses.
In animal models, exposure to cigarette smoke or nicotine during fetal development alters the expression
of the nicotinic
acetylcholine receptor in areas
of the brainstem important for autonomic
function, 28 alters the neuronal excitability
of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic
acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the normal relationship between heart rate and gestational age at birth.33 Moreover, infants
of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke alters the normal programming
of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic
function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDS.
AChE inhibitors have also been given to Alzheimer's patients in an attempt to boost
acetylcholine levels and improve cognitive
function, she says — but her research suggests that the long - term effect may be the opposite
of that intended.
Similar SH3 binding motifs exist in the formins, proteins that
function in pattern formation in embryonic limbs
of the mouse, and one subtype
of the muscarinic
acetylcholine receptor.
A Gain -
of -
Function Mutation in the α9 Nicotinic
Acetylcholine Receptor Alters Medial Olivocochlear Efferent Short - Term Synaptic Plasticity
The rationale behind the project is that
acetylcholine plays are role in cognitive
functioning and that there is a subgroup
of schizophrenia patients that have reduced density and M1 receptor binding in the hippocampus and dorsolateral prefrontal cortex that are referred to as «muscarinic receptor - deficit schizophrenia» or MRDS.
Yakel's research is directed toward understanding the role
of the nicotinic
acetylcholine receptor and brain
function, as well as how dysfunction in this receptor leads to various neurodegenerative diseases and addiction.
Here's a tantalizing prospect, hinted at by a long - running thread
of brain research: compounds that boost the
function of certain
acetylcholine circuits in the brain might also modify production
of toxic beta - amyloid protein.
The yolk
of an egg is an excellent source
of choline, a precursor to
acetylcholine, the neurotransmitter that helps to improve your focus and attention by regulating cognitive
function.
To make matters worse, as you age, you make fewer
of the chemicals your brain needs to
function properly — including the signaling brain chemical
acetylcholine, which helps support memory and cognition.
The nutrient DMAE works to maintain healthy levels
of acetylcholine, an important neurotransmitter for cognitive
function.
Brain
Function — DMAE works by accelerating the brain's synthesis
of the neurotransmitter
acetylcholine, which in turn plays a key role in maximising mental ability as well as in preventing loss
of memory in ageing adults.
Acetyl - L - Carnitine also promotes biosynthesis
of acetylcholine, a key neurotransmitter for brain and nerve
function.
This disease is caused by an inability
of the certain nerve receptors (nicotinic
acetylcholine receptors (AChRs) to
function properly.