Clinical Neurochemistry

Clinical Neurochemistry is the field of neurological biochemistry which relates biochemical phenomena to clinical symptomatic manifestations in humans.

Neuropharmagology[edit | edit source]

Cells communicate via chemical synapses.

Neurologically Active Substances[edit | edit source]

There are many biologically active chemicals which elicit an effect on the nervous system.

Excitatory and Inhibitory Amino Acids[edit | edit source]

Excitatory Amino Acids include Glutamate, whereas inhibitory Amino Acids include GABA and Glycine.

GABA Receptors[edit | edit source]

AMPA Receptors, Kainate Receptors, and NMDA Receptors

Widely Projecting Systems[edit | edit source]

Catecholamines, serotonin, acetylcholine, histaime, and orexins.

Neuropeptides[edit | edit source]

Synthesis, storage, and release. Examples include brady kinin, cholecystokinin, corticotropin-releasing factor (CRF), galanin, MCH, MSH, Neuropeptide Y (NPY), Neurotensin, Opioids, orexin, oxytocin, somatostatin, tacykinins, TRH, CUP, and vasopressin.

Atypical Neurotransmitters[edit | edit source]

Purines, endogenous cannabinoids, gasses, neurotrophix factors, chemokines, and VEGF.

Clinical Neurological Disorders[edit | edit source]

Changes in the homeostasis of many neurologically active chemicals elicit clinical disorders and symptoms.

Pain and Inflammation[edit | edit source]

Fundamentals of nociception, the pain pathways, and sensitization. Anti-inflammatory drugs, opiate drugs, and other drugs help. Damage leads to chronic pain and dorsal horn NMDA receptor plasticity.

Sleep and Arousal[edit | edit source]

Active processes in the brain, REM and non-REM sleep, circadian rhythms. Disorders such as narcolepsy, insomnia, analgesia, immobility, and hypnosis. Benzodiazepines and related drugs are the most common pharmacologic treatments.

Higher Cognitive Function and Behavior[edit | edit source]

Executive function, cognitive control of behavior, working memory, attention, dopamine D1 receptors and adronergic receptors, OCD, short and long-term memory. Structures such as the medial temporal lobe, straitum, synaptic activity, emotions. Effects of monoamines, acetylcholine, and dopamine on neurodegenerative disorders such as Alzheimer's disease or even normal aging.

Mood and Emotion[edit | edit source]

Emotions, fear, and the amygdala. Anxiety, mood disorders, genes and environmental causes, and bipolar disorder. Depression and monoamine treatment (serotonin, norepinephrine). Molecular targets, pharmacological therapies, and lithium mechanisms.

Reinforcement and Addictive Disorders[edit | edit source]

Behavior, addiction, and the reward/reinforcement pathways. VTA and NAc regions of the brain. Tolerance sensitization, dependence, addiction, tolerance, and plasticity. Effects of opiates, ethanol, nicotine, Delta-9-tetrahydrocannabinol, marijuana, PCP and ketamine. For example, cocaine is extremely addictive ^[1].

Schizophrenia and other Psychoses[edit | edit source]

Causes and symptoms of schizophrenia, including hallucinations, delisions, amotivation, social withdrawl, cognitive defects, and poor working memory. GEnetic sources, loss of gray matter, and familial effects. Treatments include antipsychotics, antischizophrenics, dopamine D2 receptor activity, and slow drug activity mechanisms.

Neurodegeneration[edit | edit source]

Alzheimer's disease and parkinson's disease are characterized by a large loss of neurons. Major processes include apoptosis and necrosis and involve mitochondrial function. Amyloid processing and dopamine loss in Alzheimers, alpha-synuclein and Parkinsons, and glutamate residues for huntingtons disease.

Seizure Disorders[edit | edit source]

Seizure classification, formation, propogation, and succession. Focal, one hemisphere, or both hemispheres. Biochemical imbalances, metabolome, and genetic analysis. Synapses involved are GABA mediated.

Stroke[edit | edit source]

Disrupted blood flow, ischemia, anoxia, and related physical phenomena. Biochemical pathways and signaling responses to low oxygen. Free radicals, apoptosis, and necrosis. Heparin treatment, and other anticoagulants.

Migraine[edit | edit source]

Migraine causes and symptoms. Cortical spreading and norepinephrine in trigeminal nerve terminals. Treatments, including prophylactic abortive strategies and triptan drugs.

See also[edit | edit source]

• Neurochemistry
• Neurotransmitter

References[edit | edit source]