lithium-chloride and Dementia

To investigate whether treatment with lithium in patients with mania or bipolar disorder is associated with a decreased rate of subsequent dementia.. Linkage of register data on prescribed lithium in all patients discharged from psychiatric health care service with a diagnosis of mania or bipolar disorder and subsequent diagnoses of dementia in Denmark during a period from 1995 to 2005.. A total of 4,856 patients with a diagnosis of a manic or mixed episode or bipolar disorder at their first psychiatric contact were included in the study. Among these patients, 2,449 were exposed to lithium (50.4%), 1,781 to anticonvulsants (36.7%), 4,280 to antidepressants (88.1%), and 3,901 to antipsychotics (80.3%) during the study period. A total of 216 patients received a diagnosis of dementia during follow-up (103.6/10,000 person-years). During the period following the second prescription of lithium, the rate of dementia was decreased compared to the period following the first prescription. In contrast, the rates of dementia during multiple prescription periods with anticonvulsants, antidepressants, or antipsychotics, respectively, were not significantly decreased compared to the rate of dementia during the period with one prescription of these drugs.. Continued treatment with lithium was associated with a reduced rate of dementia in patients with bipolar disorder in contrast to continued treatment with anticonvulsants, antidepressants, or antipsychotics. Methodological reasons for these findings cannot be excluded due to the nonrandomized nature of the data.

Topics: Adult; Aged; Antidepressive Agents; Antimanic Agents; Antipsychotic Agents; Bipolar Disorder; Dementia; Denmark; Evidence-Based Medicine; Female; Follow-Up Studies; Humans; Lithium Chloride; Male; Middle Aged; Registries; Regression Analysis; Retrospective Studies

Tau protein hyperphosphorylation and aggregation into neurofibrillary tangles are characteristic features of several neurodegenerative disorders referred to as tauopathies. Among them, frontotemporal dementia and Parkinsonism linked to chromosome 17 may be caused by dominant missense mutations in the tau gene. Transgenic mice expressing mutant tau serve as valid model systems to study the ethiopathogenesis of these diseases and assay possible therapeutic interventions. Here we report that chronic lithium treatment of a transgenic mouse strain expressing human tau with three missense mutations results in decreased glycogen synthase kinase-3-dependent-tau phosphorylation and a reduction of filamentous aggregates. These data indicate that lithium, presumably acting through the inhibition of glycogen synthase kinase 3, may be useful to curb neurodegeneration in tauopathies.

Topics: Animals; Brain; Dementia; Glycogen Synthase Kinase 3; Humans; Immunohistochemistry; Lithium Chloride; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Microscopy, Immunoelectron; Mutation, Missense; Neurofibrillary Tangles; Pedigree; tau Proteins; Tauopathies