top of page

Psychological Encyclopedia

Acetylcholine: Attention, Learning, and Neural Communication

4 days ago
18 min read

Author: Ukrainian Psychological Hub · Published: October 12, 2026 · Editorial Policy


Acetylcholine (ACh) is a chemical messenger used by neurons to communicate at synapses and to regulate the activity of neural circuits. In the brain, it helps shape how information is detected, selected, learned, and used; in the rest of the body, it controls crucial interactions between nerves, muscles, and autonomic organs. Its effects depend on the cells releasing it, the receptors detecting it, their timing, and the larger network in which they operate. Acetylcholine therefore has several well-established biological functions rather than one universal psychological effect. The 2023 review of basal forebrain cholinergic signaling and a 2025 systematic review of human drug studies describe both the importance of this transmitter and the limits of assigning it a single cognitive role.


For readers asking what acetylcholine does in the brain, the central answer is that it modulates attention, sensory processing, learning, memory-related encoding, behavioral flexibility, and aspects of arousal. Brain cholinergic pathways also contribute to sleep-state regulation, motivation, and interactions among other transmitter systems. These functions emerge through precisely organized connections and receptor-specific effects. Acetylcholine participates in cognitive activity; it is not a standalone measure of intelligence, alertness, memory strength, or mental health. Its role is best understood within the wider system of neurotransmission and distributed neural circuits.


What is acetylcholine?


Acetylcholine is an endogenous neurotransmitter: neurons synthesize it, store it in vesicles, release it when appropriate signals arrive, and activate specialized receptors on neighboring or nearby cells. A neuron that synthesizes and releases acetylcholine is described as cholinergic. In many peripheral synapses, it produces a comparatively direct effect, as when a motor neuron triggers skeletal muscle activity. In the brain, the same molecule can alter how populations of neurons respond to inputs, change the balance between incoming sensory information and recurrent activity, and influence whether neural activity favors detection or learning. This diversity follows from the two major receptor families, multiple receptor subtypes, and the architecture of the participating circuits Sam and Bordoni, NCBI Bookshelf.


The history of acetylcholine research also shaped neuroscience more broadly. Work on nerve-to-organ signaling helped establish the principle of chemical neurotransmission, while later receptor pharmacology distinguished rapid ion-channel responses from slower G-protein-mediated signaling. Modern methods have added anatomically selective circuit manipulations, molecular imaging, and sensors for measuring release at fine timescales. The conceptual progression is from recognizing a chemical messenger to explaining how different populations use that messenger at different moments. The review by Ballinger and colleagues traces the transition from an oversimplified diffuse arousal system toward differentiated cholinergic circuitry.


How acetylcholine signaling works


Synthesis, storage, release, and breakdown


In cholinergic nerve terminals, choline acetyltransferase synthesizes acetylcholine from choline and acetyl-CoA. The vesicular acetylcholine transporter packages the molecule into synaptic vesicles. When electrical activity reaches an appropriate terminal, calcium-dependent vesicle fusion releases ACh into the extracellular space. Released molecules encounter receptors on target neurons, glial cells, muscle cells, or other tissues according to location. Acetylcholinesterase then hydrolyzes much of the transmitter into acetate and choline; a high-affinity transporter returns choline to terminals for reuse. Consequently, the duration of a local signal reflects release, diffusion, receptor kinetics, enzyme activity, and local architecture, rather than an overall brain-wide pool of acetylcholine Physiology, Acetylcholine.


Some cholinergic effects occur at specialized close-contact synapses, whereas others extend through less geometrically restricted extracellular signaling. ACh release can be brief, tied to particular task events, or more sustained over a behavioral state. The older expression 'volume transmission' captures part of the spatial story, but treating every cholinergic projection as a diffuse spray misses target-selective connectivity. In experimental animals, temporally resolved optical probes and circuit-level recordings have revealed signaling patterns that older methods averaging over seconds or minutes could not distinguish. What these probes resolve in animals should be treated as circuit evidence requiring further human validation, not as a direct recording of acetylcholine in living human cognition Ananth et al., 2023.


Nicotinic receptors and muscarinic receptors


Nicotinic acetylcholine receptors are ligand-gated cation channels. When activated, they permit ion flow and can rapidly alter membrane potential and neurotransmitter release. Their subunit combinations matter: neuronal alpha4beta2-containing and alpha7-containing receptors, for example, differ in affinity, kinetics, calcium permeability, and location. Muscarinic receptors, M1 through M5, are G-protein-coupled receptors that influence ion channels and intracellular signaling pathways. M1, M3, and M5 generally recruit Gq/11-related pathways, while M2 and M4 generally recruit Gi/o-related pathways; the final physiological effect also depends on the cell and circuit. Both receptor families occur within the brain, and both contribute to cognition Carlson and Kraus, Cholinergic Receptors; Yakel, 2013.


The everyday labels 'excitatory neurotransmitter' and 'inhibitory neurotransmitter' become unreliable when applied to acetylcholine as a whole. Activating a nicotinic receptor can depolarize one neuron; recruiting certain muscarinic pathways can suppress a different cell's output or presynaptic release. Acetylcholine may therefore increase one neural response while reducing another, producing network-level changes that cannot be deduced from transmitter identity alone. Nor does a receptor's name tell us that nicotine or muscarine is normally required for its function: the endogenous ligand is acetylcholine. Detailed receptor pharmacology explains why drugs affecting this system can have selective intended effects and significant effects elsewhere in the body.


Where is acetylcholine made in the brain?


Basal forebrain pathways


The basal forebrain contains several major groups of cholinergic projection neurons. Medial septal and diagonal-band populations are especially important for hippocampal and related limbic circuits, while the nucleus basalis of Meynert and adjacent cell groups provide substantial cholinergic innervation to the cerebral cortex. These pathways influence many cortical operations, including task-related processing, and their organization is more structured than older anatomical diagrams implied. The exact topology varies across species and across projections. A 2025 account of the human basal forebrain describes its Ch1–Ch4 group organization and regional patterns of innervation; the 2023 Nature Reviews Neuroscience synthesis reviews circuit specificity and cognitive functions.


Anatomical projections and functional effects should be distinguished. A region containing many cholinergic terminals may be capable of strong modulation without every nearby psychological operation depending on those terminals. The basal forebrain itself also contains noncholinergic neurons, including GABAergic and glutamatergic cell populations. Stimulating an entire anatomical region can thus recruit several signaling systems at once. Modern studies try to isolate molecularly defined cells and projections, yet outcomes may still depend on behavioral task, stimulation timing, and species. Cortical acetylcholine acts within attention and association networks rather than supplying a separate cognition center Ballinger et al., 2016.


Brainstem pathways and local interneurons


Cholinergic neurons in the pedunculopontine and laterodorsal tegmental regions participate in brainstem and subcortical signaling, projecting to targets that include the thalamus and midbrain. Their effects intersect with sleep-wake regulation, sensory processing, movement, and other neuromodulatory systems. Within the striatum, important cholinergic signaling also comes from local interneurons, which help regulate the activity of projection neurons and interactions with dopamine. It is therefore inaccurate to imagine one central acetylcholine source or one identical function across cortex, hippocampus, thalamus, and basal ganglia. The relevant question is which cholinergic population, receptor subtype, target circuit, and behavior a finding concerns Ananth et al., 2023; Wittenberg et al., 2020.


What does acetylcholine do for attention?


Attention requires selecting behaviorally useful signals while maintaining appropriate responsiveness to the environment. Acetylcholine is one contributor to this selection. Animal experiments have linked cortical cholinergic signaling to detecting relevant cues, responding to distractors, and adjusting processing under demanding conditions. Human pharmacological experiments and neuroimaging add convergent evidence, although direct measurement of fast ACh release during human tasks remains constrained. The 2025 systematic review by Dan, Christakou, and Roelofs identifies evidence concerning sustained attention, perceptual detection, information-processing speed, and updating cue-response relationships; it also emphasizes that drug effects differ by receptor class and experimental design.


A useful mechanistic description is signal prioritization. Depending on the circuit, ACh can modify the responsiveness of sensory and association pathways, the strength of particular synaptic inputs, and the probability that task-relevant information receives further processing. Prefrontal control systems, cortical sensory regions, basal forebrain neurons, and wider task networks contribute to this coordination. Some experiments distinguish transient cholinergic responses to a detected cue from slower state-related changes. Those patterns support a role in attentional control, but they do not prove that acetylcholine determines subjective concentration on its own. For context, Chakraborty and colleagues' human meta-analysis reported spatial and behavioral evidence involving midcingulo-insular attention-related regions.


The distinction between sustained attention, orienting, selective attention, and vigilance matters. Behavioral tasks operationalize these capacities differently, and the same drug can improve one measure while worsening or failing to change another. Further, better speed does not always mean better accuracy, and a brain activation shift does not necessarily signify improvement. The 2025 human systematic review reported heterogeneous effects of nicotinic and muscarinic manipulation, including results that resist the simplistic prediction that increasing all cholinergic activity will enhance cognition. These observations also limit casual comparisons between acetylcholine, norepinephrine, and dopamine as if each corresponded to one discrete mental faculty Dan et al., 2025.


How does acetylcholine contribute to learning and memory?


Learning involves coordinated changes in neural activity and connections distributed across many brain structures. Acetylcholine helps regulate some of the conditions under which information can be encoded, including attention to incoming input, excitability of relevant cells, and synaptic plasticity. In hippocampal and cortical models, cholinergic signaling can alter the balance between afferent input and recurrent feedback, potentially favoring the encoding of new information under certain conditions. Experiments with receptor blockers, selective circuit perturbations, and electrophysiology support such roles. They do not justify assigning all memory storage to acetylcholine, and they do not imply a universal relationship between concentration of the transmitter and performance Hasselmo, 2006.


The hippocampus works with several cortical and subcortical systems during memory formation, contextual processing, and navigation. Cholinergic inputs from medial septal and diagonal-band populations can influence local interneurons, hippocampal principal neurons, synaptic dynamics, and neural rhythms. Some animal work suggests that individual basal forebrain cell groups make distinguishable contributions to object and spatial recognition. This specificity is scientifically useful because a deficit on one laboratory task does not mean that every form of memory is globally impaired. The link between ACh and hippocampal function is supported by receptor studies and circuit research, while the precise translation of task-level animal effects to diverse human memories remains an active question Yakel, 2013; Ballinger et al., 2016.


Plasticity is the capacity of neural connections and circuits to change with experience and activity. ACh can alter conditions for long-term potentiation and other changes, but actual learning depends on the timing of activity, circuit architecture, other neurotransmitters, prior knowledge, sleep, and subsequent experience. One influential model proposes that higher cholinergic states favor encoding new inputs over internally generated retrieval; this is a specific model, not a universally established switch separating learning from remembering. Research has increasingly emphasized the coordination of neural populations over time. The broader evidence for adaptive brain change is reviewed in Neuroplasticity: How the Brain Changes Through Experience and in Ananth et al., 2023.


Acetylcholine in arousal, sleep, movement, and reward


Acetylcholine participates in the regulation of wakefulness and rapid eye movement (REM) sleep through interactions among basal forebrain, brainstem, thalamic, cortical, and hypothalamic circuits. Cholinergic activity and release can vary with behavioral state; specific older microdialysis experiments showed greater measured release in waking and REM than in non-REM sleep in an animal model. Such findings support state dependence but do not imply that acetylcholine alone induces sleep or dreams. REM sleep and waking arise from coordinated populations using multiple transmitters, and cholinergic manipulation has different effects depending on site and receptor. Research into lucid dreaming remains particularly preliminary and cannot support general pharmacological recommendations Sleep-wake circuitry review; Acetylcholine and metacognition during sleep.


In movement, ACh operates through several distinct routes. At the neuromuscular junction, motor neurons release it onto muscle-type nicotinic receptors, initiating events that produce skeletal muscle contraction. Within motor-related brain networks, local cholinergic interneurons in the striatum contribute to the regulation of action selection and learning together with dopamine-dependent mechanisms. These functions belong to different levels of organization. A person's strength, movement speed, or motivation cannot be inferred from a presumed global acetylcholine level; such measures reflect neuromuscular integrity, circuit health, task conditions, and many other physiological influences Physiology, Acetylcholine.


Reward research also makes the receptor distinction important. Nicotinic ACh receptors occur on neurons that communicate using dopamine, GABA, and glutamate, and their activation can alter activity in the ventral tegmental area and related circuits. Nicotine, an external substance, binds some of these receptors and can induce adaptations associated with dependence. This does not make endogenous acetylcholine equivalent to nicotine or make it a universal 'pleasure chemical.' Reward-related behavior emerges from interacting cortical, striatal, midbrain, and other networks. Wittenberg and colleagues' review outlines receptor-specific nicotine effects; the Brain Reward System explains the wider circuit-level picture.


What acetylcholine does outside the brain


Acetylcholine is equally indispensable in the peripheral nervous system. At the skeletal neuromuscular junction it transmits motor commands to muscle; in the autonomic nervous system, it is released by preganglionic neurons in both major autonomic divisions and by most parasympathetic postganglionic neurons. Certain sympathetic postganglionic pathways, such as those to sweat glands, are also cholinergic. Receptor localization helps explain effects on heart rate, glandular secretion, gastrointestinal motility, pupil responses, urination, and other organ functions. A drug that changes muscarinic signaling may therefore cause dry mouth, constipation, urinary difficulties, or changes in heart rhythm alongside any central effect. These functions are documented in NIH's acetylcholine physiology chapter.


At the neuromuscular junction, some diseases affect the effectiveness of acetylcholine signaling or the structures that respond to it. This is a separate clinical context from the regulation of attention and memory by brain circuits. For example, a receptor-mediated neuromuscular problem produces characteristic patterns of muscle weakness rather than a generic 'low acetylcholine brain' syndrome. The chemical's use in different organs demonstrates why symptoms alone cannot reliably disclose its concentration or point to a single biological cause. Diagnosis requires a clinical history, appropriate examination, and condition-specific testing where indicated.


How scientists study acetylcholine


The strongest mechanistic explanations combine evidence across research methods. Biochemical assays and immunohistochemistry identify enzymes, receptor distributions, or cholinergic structures in tissue, often postmortem in human neuroanatomy. Electrophysiology records neuronal electrical behavior, not the transmitter concentration itself. Microdialysis samples extracellular chemicals but ordinarily integrates activity over comparatively long time windows. Rapid optical fluorescent sensors in animals can report changes in locally detected transmitter-related fluorescence with finer temporal detail; signal interpretation depends on sensor calibration and tissue context. Optogenetic or chemogenetic interventions in suitable animal models can test the consequences of manipulating selected cells, but their findings concern the manipulated cells and animals studied Ananth et al., 2023.


Human experiments use pharmacological perturbation, behavioral tasks, anatomical MRI, functional MRI, and specialized positron emission tomography (PET). Administering a cholinergic drug can strengthen a causal argument about a pharmacological manipulation and a measured outcome, yet most drugs act at multiple sites, have peripheral effects, and may fail to reproduce naturally timed release. Functional MRI predominantly measures blood-oxygenation-dependent hemodynamic changes associated with neural activity; it does not measure acetylcholine molecules. Structural MRI depicts anatomy and cannot establish neurotransmitter release. PET radiotracers can target selected receptor or transporter systems but require careful interpretation: tracer binding or terminal markers cannot automatically be converted into moment-by-moment synaptic neurotransmitter concentrations. The Brain Imaging Methods guide explains these measurement boundaries.


For example, FEOBV PET research uses a ligand related to the vesicular acetylcholine transporter to estimate cholinergic terminal integrity. A small human study reported group-level differences associated with cognitive impairment; the evidence remains an association in selected participants, not a validated standalone test for an individual person's memory ability. Human meta-analytic neuroimaging research also finds relationships between cholinergic modulation and attention-related networks, but pooled activation patterns cannot show that a single cortical node causes an entire psychological capacity. A region's activation during a task is compatible with multiple cognitive explanations. This restriction is central to avoiding reverse inference.


What the evidence establishes—and what remains under investigation


Well-established physiological evidence supports acetylcholine as a neurotransmitter with two receptor families, rapid synaptic functions at the neuromuscular junction, important autonomic effects, and major central cholinergic projections. Converging evidence supports a role in multiple cognitive processes, especially attention-related processing and learning-related circuit regulation. The precise magnitude, direction, and necessity of any effect vary by receptor, task, location, age, and health status. The strongest recent human synthesis is the 2025 systematic review, which confirms differentiated cognitive effects while documenting limitations of drug selectivity and the challenge of matching pharmacological interventions to natural signal dynamics.


More specific proposals remain active research programs. One prominent computational account suggests that cholinergic signals help regulate the influence of incoming information relative to prior predictions when cues are unreliable. The influential Yu and Dayan model assigns acetylcholine a role in expected uncertainty and norepinephrine a different role in unexpected changes. This is a theoretical framework offering testable predictions; it is not direct proof that a human brain encodes a single 'uncertainty value' in acetylcholine concentration. Competing accounts stress sensory gain, cue detection, learning-state control, attention, and circuit-specific coordination. Contemporary reviews increasingly integrate rather than assume a single global computational function.


A further challenge is translation between species. Rodent work permits projection-specific manipulation and direct chemical sensing unavailable in routine human research. Human cortex differs in scale, anatomy, and experimental accessibility. Animal causal demonstrations support plausible neural mechanisms and guide research; they do not in themselves establish equivalent human clinical effects. Neuroimaging can suggest where cholinergic pathways matter in people while remaining indirect or correlational in key respects. Strong inference therefore requires triangulation, replication, appropriate controls, and clarity about which variable each method measures Geula et al., 2025; Ananth et al., 2023.


Clinical relevance: Alzheimer's disease and medication effects


The cholinergic hypothesis of cognitive decline grew partly from observations of degeneration in basal forebrain systems and changes in cholinergic markers associated with Alzheimer's disease. These observations identify one meaningful component of disease biology. Alzheimer's pathology includes multiple interacting processes and cannot be reduced to a simple shortage of acetylcholine. Cholinesterase inhibitors such as donepezil, rivastigmine, and galantamine slow the enzymatic breakdown of ACh and can help manage selected cognitive or behavioral symptoms in some patients. They do not establish that the entire disease is caused by one missing chemical. The National Institute on Aging's treatment overview distinguishes symptom-directed medications from treatments targeting disease mechanisms.


It is also important to separate group-level biomedical research from individual diagnosis. Changes in cholinergic structure, receptor availability, or PET binding may be useful research biomarkers, and they can correlate with cognitive differences in selected samples. Their predictive usefulness, measurement reliability, specificity, and clinical thresholds require independent validation before any marker becomes a personal diagnostic test. Memory complaints can have numerous explanations, including sleep problems, medication effects, mood symptoms, and medical conditions. A person's perceived focus or forgetfulness cannot be used to diagnose cholinergic deficiency Berry and Harrison, 2023; FEOBV imaging study.


Drugs with anticholinergic properties can interfere with acetylcholine-dependent signaling. Depending on the compound, dose, duration, age, and context, unwanted effects may include impaired attention, confusion, dry mouth, constipation, or urinary retention. Observational research has found associations between greater anticholinergic medication exposure and later dementia outcomes, including in a systematic review and meta-analysis. Observational associations do not by themselves prove that medication exposure caused dementia: underlying illnesses, prescribing patterns, and other confounders matter. Medication reviews should be individualized with a qualified clinician; abruptly stopping prescribed treatment based on a population association can create additional risks.


Acetylcholine also appears in the pathophysiology and pharmacology of several neurologic and neuromuscular conditions, but each has distinct causes, criteria, and treatments. Drugs influencing nicotinic or muscarinic receptors, cholinesterase activity, and peripheral transmission can produce substantial systemic effects. Research on stimulating basal forebrain pathways and other cholinergic interventions does not create a general recommendation for self-directed cognitive enhancement, unprescribed drug use, or neurostimulation. Clinical decisions require condition-specific evidence and professional monitoring.


Can diet, supplements, or everyday activities increase acetylcholine?


Choline is a nutrient and a biochemical precursor used in acetylcholine synthesis; the body also uses it for cell membranes and other functions. Adequate nutrition matters for normal physiology. Yet providing more dietary precursor does not guarantee a proportional increase in synaptic release or better attention, because synthesis and release are controlled at multiple cellular and circuit levels. People with different nutritional states may respond differently, and studies of supplements must distinguish correcting deficiency from enhancing performance in well-nourished healthy adults. A systematic review of commonly marketed cognitive supplements described low certainty across much of the evidence and insufficient grounds for broad enhancement recommendations.


Sleep, physical activity, learning opportunities, and environmental conditions can influence cognitive functioning through many interacting mechanisms. It is scientifically misleading to explain the value of these activities as a proven, selective boost to brain acetylcholine. Commercial 'acetylcholine boosters' often mix precursor claims, in vitro results, animal experiments, and heterogeneous clinical outcomes into a single untested promise. Any supplement proposal requires product-specific evidence, a defined population, meaningful clinical or behavioral endpoints, and safety assessment. Nicotine activates nicotinic ACh receptors but brings dependence and health risks and is not a general attention-treatment strategy Wittenberg et al., 2020.


Acetylcholine myths and common misunderstandings


The claim that acetylcholine is simply 'the memory chemical' conflates a necessary family of neuromodulatory contributions with the distributed biological processes that make memory possible. The statement that more acetylcholine always means better learning fails to consider inhibitory receptor effects, differences among tasks, and the nonlinear consequences of changing network states. The opposite claim, that low acetylcholine is the explanation for every lapse in concentration, assumes a biomarker that routine symptoms cannot supply. Nor can one brain scan read someone's acetylcholine 'level': methods measure structure, hemodynamics, tracer uptake, or related biological signals, with distinct strengths and limitations Dan et al., 2025; Chakraborty et al., 2024.


Another persistent misconception is that a neurotransmitter has exactly one emotional or cognitive assignment. Acetylcholine intersects with noradrenergic signaling in attention, dopaminergic systems in action selection and reward, glutamatergic and GABAergic local circuits in synaptic regulation, and neuromodulatory mechanisms linked to sleep and arousal. The correct level of explanation depends on the question: chemical synthesis for neurotransmission, receptor pharmacology for drug effects, pathways for neuroanatomy, controlled tasks for behavior, and clinically validated methods for care. These levels are connected; none can substitute for the others.


Frequently asked questions


What is the main function of acetylcholine in the brain?


Its central role is to regulate neural communication in ways that support attention, sensory selection, learning, memory-related processing, and behavioral-state coordination. Different cholinergic pathways and receptor types exert different effects, so no single cognitive phrase captures every function Ananth et al., 2023.


Does acetylcholine help you concentrate?


Research connects cholinergic signaling with cue detection, sustained attention, and processing of relevant information. Effects differ across circumstances and interventions, and individual concentration is influenced by numerous systems. Human pharmacological results support involvement without validating a simple 'more equals more focus' rule Dan et al., 2025.


How is acetylcholine different from dopamine?


They are distinct signaling molecules with different synthesis, receptors, cellular pathways, and distributions. Acetylcholine is involved in neuromuscular and autonomic transmission as well as central modulation; dopamine contributes importantly to movement and reinforcement-related learning, among other roles. They interact in striatal and midbrain circuits. Neither molecule corresponds to one feeling or a single behavioral goal Wittenberg et al., 2020.


What is the difference between acetylcholine and choline?


Choline is a nutrient and biochemical building block. Acetylcholine is synthesized from choline and acetyl-CoA and acts as a transmitter at cholinergic signaling sites. Consuming choline supports nutritional needs but does not ensure a specific short-term increase in cognitive performance Sam and Bordoni.


What happens if acetylcholine signaling is blocked?


The result depends on where and which receptors or enzymes are affected. Blocking certain central muscarinic functions can disrupt attention or memory performance; blocking receptors at the neuromuscular junction affects muscle activation; peripheral muscarinic blockade may alter secretions, digestion, or heart-related functions. Such effects require medically specific interpretation, not a generalized 'brain chemical imbalance' diagnosis Carlson and Kraus.


Can acetylcholine be measured by a blood test or standard brain scan?


A routine blood result or conventional MRI cannot determine functional acetylcholine signaling in an individual's brain. Specialized research methods can examine certain receptor or transporter features and animal studies can measure local transmitter dynamics. These are different constructs and cannot be treated as a validated everyday diagnosis of poor attention or memory FEOBV PET study.


Is acetylcholine associated with Alzheimer's disease?


Yes. Basal forebrain cholinergic changes are part of the neurobiology studied in Alzheimer's disease, and cholinesterase inhibitors may provide symptomatic benefit for some people. The disease involves several pathological processes and needs a proper clinical evaluation rather than assumptions about a single neurotransmitter National Institute on Aging.


Do acetylcholine supplements improve memory?


There is no general clinical conclusion that marketed acetylcholine-raising supplements reliably improve memory in healthy adults. Studies differ by compound, dose, population, and endpoint, and precursor availability alone does not specify synaptic function. Decisions about supplementation should reflect nutritional and medical context, rather than promotional neurochemical narratives systematic supplement review.


Related articles



Related Articles





References

Ananth, M. R., Rajebhosale, P., Kim, R., Talmage, D. A., & Role, L. W. (2023). Basal forebrain cholinergic signalling: Development, connectivity and roles in cognition. Nature Reviews Neuroscience, 24, 233–251. https://doi.org/10.1038/s41583-023-00677-x.

Ballinger, E. C., Ananth, M., Talmage, D. A., & Role, L. W. (2016). Basal forebrain cholinergic circuits and signaling in cognition and cognitive decline. Neuron, 91, 1199–1218. https://doi.org/10.1016/j.neuron.2016.09.006.

Berry, A. S., & Harrison, T. M. (2023). New perspectives on the basal forebrain cholinergic system in Alzheimer's disease. Neuroscience & Biobehavioral Reviews, 150, 105192. https://doi.org/10.1016/j.neubiorev.2023.105192.

Carlson, A. B., & Kraus, G. P. (2023). Physiology, cholinergic receptors. StatPearls, NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK526134/.

Chakraborty, S., Lee, S. K., Arnold, S. M., Haast, R. A. M., Khan, A. R., & Schmitz, T. W. (2024). Focal acetylcholinergic modulation of the human midcingulo-insular network during attention: Meta-analytic neuroimaging and behavioral evidence. Journal of Neurochemistry, 168, 397–413. https://doi.org/10.1111/jnc.15990.

Crawford, C., Boyd, C., & Deuster, P. A. (2021). Dietary supplement ingredients for optimizing cognitive performance among healthy adults: A systematic review. Journal of Alternative and Complementary Medicine, 27(11), 940–958. https://doi.org/10.1089/acm.2021.0135.

Dan, Y. R., Christakou, A., & Roelofs, K. (2025). Systematic review: Effects of cholinergic signaling on cognition in human pharmacological studies. Neuroscience & Biobehavioral Reviews, 179, 106408. https://doi.org/10.1016/j.neubiorev.2025.106408.

Geula, C., Ayala, I., Gefen, T., & Mesulam, M.-M. (2025). Organization of the basal forebrain cholinergic system in the human brain. Handbook of Clinical Neurology, 211, 11–21. https://doi.org/10.1016/B978-0-443-19088-9.00009-3.

Gott, J. A., Stücker, S., Kanske, P., Haaker, J., & Dresler, M. (2024). Acetylcholine and metacognition during sleep. Consciousness and Cognition, 117, 103608. https://doi.org/10.1016/j.concog.2023.103608.

Hasselmo, M. E. (2006). The role of acetylcholine in learning and memory. Current Opinion in Neurobiology, 16, 710–715. https://doi.org/10.1016/j.conb.2006.09.002.

National Institute on Aging. How is Alzheimer's disease treated? https://www.nia.nih.gov/health/alzheimers-treatment/how-alzheimers-disease-treated.

Sam, C., & Bordoni, B. (2023). Physiology, acetylcholine. StatPearls, NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK557825/.

Wittenberg, R. E., Wolfman, S. L., De Biasi, M., & Dani, J. A. (2020). Nicotinic acetylcholine receptors and nicotine addiction: A brief introduction. Neuropharmacology, 177, 108256. https://doi.org/10.1016/j.neuropharm.2020.108256.

Xia, Y., Eeles, E., Fripp, J., et al. (2022). Reduced cortical cholinergic innervation measured using [18F]-FEOBV PET imaging correlates with cognitive decline in mild cognitive impairment. NeuroImage: Clinical, 34, 102992. https://doi.org/10.1016/j.nicl.2022.102992.

Yakel, J. L. (2013). Cholinergic receptors: Functional role of nicotinic ACh receptors in brain circuits and disease. Pflügers Archiv, 465, 441–450. https://doi.org/10.1007/s00424-012-1200-1.

Yu, A. J., & Dayan, P. (2005). Uncertainty, neuromodulation, and attention. Neuron, 46, 681–692. https://doi.org/10.1016/j.neuron.2005.04.026.

Zaborszky, L., & Duque, A. (2003). Sleep-wake mechanisms and basal forebrain circuitry. Frontiers in Bioscience, 8, d1146–d1169. https://doi.org/10.2741/1112.

Zheng, Y.-B., Shi, L., Zhu, X.-M., et al. (2021). Anticholinergic drugs and the risk of dementia: A systematic review and meta-analysis. Neuroscience & Biobehavioral Reviews, 127, 296–306. https://doi.org/10.1016/j.neubiorev.2021.04.031.

 
 
bottom of page