biomarker, bipolar disorder, dendritic spine loss, dendritic spines, dorsolateral prefrontal cortices, healthinnovations, neuroinnovations, schizophrenia

Schizophrenia, bipolar disorder linked with dendritic spine loss in brain.

Researchers from Harvard University and McLean Hospital have shown that schizophrenia and bipolar disorder both appear to be associated with dendritic spine loss in the brain, suggesting the two distinct disorders may share common neuropsychiatric features.

Schizophrenia is one of the most common serious mental health conditions. About 1 in 100 people will experience schizophrenia in their lifetime, with many continuing to lead normal lives. It is a long-term mental health condition that causes a range of different symptoms such as delusions, and hallucinations.  Schizophrenia is caused by a combination of genetic and environmental factors and can be treated using antipsychotic medicines and cognitive behavioural therapy.

Bipolar disorder is a condition which causes a person’s mood to swing extremely between depression and mania.  Extreme stress, overwhelming problems and life-changing events, as well as genetic and chemical factors are thought to cause bipolar disorder which effects one in every 100 adults at some point in their lives.  Medications, including antipsychotics, and talkative therapies are used to treat a bipolar personality.

The dendritic spines play a role in a variety of brain functions. Previous studies have observed spine loss in the dorsolateral prefrontal cortices (DLPFCs) from individuals with schizophrenia. To determine whether spine pathology happens in individuals with a disorder distinct from schizophrenia, the study included patients with bipolar disorder in their study.  Schizophrenia and bipolar disorder differ clinically but they share many features.

The researchers analyzed postmortem human brain tissue from 14 individuals with schizophrenia, nine individuals with bipolar disorder and 19 unaffected control group individuals.

The team found that average spine density was reduced in individuals with bipolar disorder by 10.5 percent and in individuals with schizophrenia by 6.5 percent compared with control patients.

There was a significant reduction in the average number of spines per dendrite in both individuals with schizophrenia who had on average, 72.8 spines per dendrite, and individuals with bipolar disorder who had on average, 68.9 spines per dendrite; compared with control group individuals who were found to have on average, 92.8 spines per dendrite. Individuals with schizophrenia and bipolar disorder also had reduced average dendrite length compared with the control group.

This could suggest a regrowth dendrites to compensate for the loss of dendritic spine cover, this could also explain the negligible amount of overall spine density compared to the significant lack of dendritic spines per dendrite.  This ‘dendritic-genesis’ may therefore be viewed as an ‘overgrowth’ and detrimental to the subject.

Overall the current study suggests that spine pathology is common to both schizophrenia and bipolar disorder and that the study of the mechanisms underlying the spine pathology might reveal additional similarities and differences between the two disorders, which could lead to the development of novel biomarkers and therapeutics.

Source:  JAMA Psychiatry

 

(a) Represents the first Cajal scientific drawing showing dendritic spines from a Purkinje cell of the hen, 1888. Inset shows dendritic spines digitally enlarged of the boxed region. (b) Purkinje cell and dendritic spines (inset) of the adult bird cerebellum taken from a Cajal's histological preparation stained following the Golgi method. (c) drawing by Cajal [5] showing dendritic spines of pyramidal (A), Purkinje (B), basket (C) and Golgi cells (D). (d) dendritic spines and filopodia taken from Cajal histological preparations, and Golgi impregnation; 1, dendritic spines, pyramidal cell, parietal cortex, one-month-old human; 2, dendritic spines, Purkinje cell, adult cat cerebellum; 3, dendritic filopodia and spines, basket cell, cerebellum, of 17-day-old dog; 4, Golgi cell dendrite, cerebellum, of 17-day-old dog. Freire et al 2011.
(a) Represents the first Cajal scientific drawing showing dendritic spines from a Purkinje cell of the hen, 1888. Inset shows dendritic spines digitally enlarged of the boxed region. (b) Purkinje cell and dendritic spines (inset) of the adult bird cerebellum taken from a Cajal’s histological preparation stained following the Golgi method. (c) drawing by Cajal [5] showing dendritic spines of pyramidal (A), Purkinje (B), basket (C) and Golgi cells (D). (d) dendritic spines and filopodia taken from Cajal histological preparations, and Golgi impregnation; 1, dendritic spines, pyramidal cell, parietal cortex, one-month-old human; 2, dendritic spines, Purkinje cell, adult cat cerebellum; 3, dendritic filopodia and spines, basket cell, cerebellum, of 17-day-old dog; 4, Golgi cell dendrite, cerebellum, of 17-day-old dog. Freire et al 2011.

 

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