142 research outputs found
Lithium suppression of tau induces brain iron accumulation and neurodegeneration
Lithium is a first-line therapy for bipolar affective disorder. However, various adverse effects, including a Parkinson-like hand tremor, often limit its use. The understanding of the neurobiological basis of these side effects is still very limited. Nigral iron elevation is also a feature of Parkinsonian degeneration that may be related to soluble tau reduction. We found that magnetic resonance imaging T2 relaxation time changes in subjects commenced on lithium therapy were consistent with iron elevation. In mice, lithium treatment lowers brain tau levels and increases nigral and cortical iron elevation that is closely associated with neurodegeneration, cognitive loss and parkinsonian features. In neuronal cultures lithium attenuates iron efflux by lowering tau protein that traffics amyloid precursor protein to facilitate iron efflux. Thus, tau- and amyloid protein precursor-knockout mice were protected against lithium-induced iron elevation and neurotoxicity. These findings challenge the appropriateness of lithium as a potential treatment for disorders where brain iron is elevated (for example, Alzheimer’s disease), and may explain lithium-associated motor symptoms in susceptible patients
Review Article - Botulinum toxins: Pharmacology and its current therapeutic evidence for use
Botulinum toxins are, as a group, among the most potent neuromuscular
toxins known, yet they are clinically useful in the management of
conditions associated with muscular and glandular over-activity.
Botulinum toxins act by preventing release of acetylcholine into the
neuromuscular junction. While botulinum toxin type A is commonly
available, different manufacturers produce specific products, which are
not directly interchangeable and should not be considered as
generically equivalent formulations. Type B is also available in the
market. Each formulation of botulinum toxin is unique with distinct
dosing, efficacy and safety profiles for each use to which it is
applied. Botulinum toxin type A is the treatment of choice based on its
depth of evidence in dystonias and most other conditions. Botulinum
toxin type A is established as useful in the management of spasticity,
tremors, headache prophylaxis and several other neurological
conditions. Active research is underway to determine the parameters for
which the type B toxin can be used in these conditions, as covered in
this review. Botulinum toxin use has spread to several fields of
medicine
Review Article - Botulinum toxins: Pharmacology and its current therapeutic evidence for use
Botulinum toxins are, as a group, among the most potent neuromuscular
toxins known, yet they are clinically useful in the management of
conditions associated with muscular and glandular over-activity.
Botulinum toxins act by preventing release of acetylcholine into the
neuromuscular junction. While botulinum toxin type A is commonly
available, different manufacturers produce specific products, which are
not directly interchangeable and should not be considered as
generically equivalent formulations. Type B is also available in the
market. Each formulation of botulinum toxin is unique with distinct
dosing, efficacy and safety profiles for each use to which it is
applied. Botulinum toxin type A is the treatment of choice based on its
depth of evidence in dystonias and most other conditions. Botulinum
toxin type A is established as useful in the management of spasticity,
tremors, headache prophylaxis and several other neurological
conditions. Active research is underway to determine the parameters for
which the type B toxin can be used in these conditions, as covered in
this review. Botulinum toxin use has spread to several fields of
medicine
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