Abstract
Alzheimer's disease (AD) is characterized by disruptions in multiple major neurotransmitters. While many studies have attempted to establish whether GABA is disrupted in AD patients, findings have varied. We review evidence for disruptions in GABA among patients with AD and suggest that the variable findings reflect subtypes of the disease that are possibly manifested clinically by differing behavioural symptoms. GABA, the major inhibitory neurotransmitter, has long been a target for anxiolytics, hypnotic sedatives, and anticonvulsants. We review the clinical use of GABAergic agents in treating persons with AD symptoms. While newer generation GABAergic medications are now available, they have yet to be evaluated among patients with AD.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Aged
-
Alzheimer Disease / drug therapy*
-
Alzheimer Disease / physiopathology*
-
Benzodiazepines / pharmacokinetics
-
Benzodiazepines / therapeutic use
-
Binding Sites
-
Brain / blood supply
-
Brain / metabolism
-
Brain / physiopathology*
-
Frontal Lobe / blood supply
-
Frontal Lobe / metabolism
-
Frontal Lobe / physiopathology
-
GABA Agonists / classification
-
GABA Agonists / pharmacokinetics
-
GABA Agonists / therapeutic use*
-
Humans
-
Limbic System / blood supply
-
Limbic System / metabolism
-
Limbic System / physiopathology
-
Parietal Lobe / blood supply
-
Parietal Lobe / metabolism
-
Parietal Lobe / physiopathology
-
Receptors, GABA / physiology
-
Temporal Lobe / blood supply
-
Temporal Lobe / metabolism
-
Temporal Lobe / physiopathology
-
Tomography, Emission-Computed
-
Tomography, Emission-Computed, Single-Photon
-
gamma-Aminobutyric Acid / metabolism
-
gamma-Aminobutyric Acid / physiology*
Substances
-
GABA Agonists
-
Receptors, GABA
-
Benzodiazepines
-
gamma-Aminobutyric Acid