Abnormal proteins linked to aggressive behavior among dementia patients

In a recent study, scientists have observed an association between certain proteins and  dementia sufferers` tendency, to commit criminal acts. The research studied deceased patients who were diagnosed with Alzheimer's disease Alzheimer's disease or frontotemporal dementia. “This study is unique in that we studied deceased patients, something that means we are 100 per cent sure of the dementia diagnosis, which is not always established while the patients are alive,” said a researcher.

“In addition, we observed that the likelihood of committing criminal acts was nine times higher among patients with frontotemporal dementia who had accumulations in the brain of certain abnormal proteins, above all TDP-43, compared with those who had accumulations of tau protein. The TDP-43 proteins seem therefore to be particularly associated with developing criminal behaviour among people with frontotemporal dementia,” she added.

When a person who previously has been perceived by those around them as well-behaved starts committing criminal acts such as theft, shoplifting, sexual harassment or other aggressive behaviours, there may be a dementia disease behind these unexpected actions. Researchers in the Neuropathology team studied 220 deceased patients with Alzheimer`s disease or frontotemporal dementia (FTD), who had been monitored at the Clinic between 1967 and 2017.

Of these, 30 per cent had committed a criminal offence – 15 per cent of the total number of patients who had Alzheimer`s and 42 per cent among those who had FTD. The latter group committed repeated criminal offences to a greater extent than the Alzheimer`s group. When examining the behaviour such as excessively loud laughing or unexpected shouting, the frontotemporal dementia group is also over-represented (75 per cent), compared with the Alzheimer`s group (56 per cent). “It confirms what we have seen in previous studies.

With these patients, the damage is in the frontal part of the brain, where our personality, including impulse control and empathy, resides”, said a Dr., emphasising that dementia diseases do not exclusively affect the elderly. “Frontotemporal dementia can also occur in younger people and it can often take a long while before there is a correct diagnosis. That is why it`s important that relatives, healthcare services, the police and the entire legal system respond to altered social and criminal behaviour and provide assistance to enable these people to get medical care”, she concluded.

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Dysfunction in brain structure may cause Huntington's disease

Dysfunction of a group of brain structures critical for movement and impulse control may be behind Huntington's disease, according to a new study that could lead to a therapy for the currently incurable disorder.
 
Scientists at Northwestern University in the US identified a link between Huntington's disease and dysfunction of the sub-thalamic nucleus, a component of the basal ganglia, a group of brain structures critical for movement and impulse control. Huntington's disease is characterised by the progressive loss of nerve cells in the brain and affects about one in 10,000 people. This fatal disorder is caused by a hereditary defect in a single gene.

"Although the genetic basis of the disease is well established, why the mutation leads to the expression of symptoms and loss of brain tissue remains poorly understood," said Mark Bevan, professor of physiology at Northwestern University Feinberg School of Medicine. The debilitating symptoms of Huntington's disease typically manifest in adulthood and involve loss of motor and cognitive function, depression and personality changes.

From the point of onset, symptoms develop and intensify over the following 10 to 25 years until death, typically due to complications associated with the disease.

"While research into Huntington's disease has focused on other parts of the basal ganglia, the sub-thalamic nucleus has been largely overlooked," said Bevan.

"This is surprising because patients with Huntington's disease have fewer nerve cells in the sub-thalamic nucleus. People who have suffered damage to the sub-thalamic nucleus exhibit excessive movement and impulsive behaviour, similar to patients with Huntington's disease," he said.

Using mice genetically engineered to carry the Huntington's disease gene, scientists discovered the electrical activity of the subthalamic nucleus was lost.

Impaired subthalamic activity was caused by anomalous receptor signalling, leading to defective energy metabolism and accumulation of damaging oxidants.

The researchers also found abnormalities in the sub-thalamic nucleus occur earlier than in other brain regions, and that sub-thalamic nucleus nerve cells progressively degenerate as the mice age, mirroring the human pathology of
Huntington's disease. "Our findings suggest early problems in the sub-thalamic

nucleus not only contribute to the symptoms of Huntington's disease, but are also likely to impair the processing capacity and health of other brain structures, more traditionally associated with the disease," Bevan said.

Currently, there is no cure for Huntington's disease; treatment can only alleviate some of the symptoms. A better understanding of aberrant brain receptor signalling that leads to nerve cell dysfunction could reveal a target for therapy, researchers said. 

The study was published in the journal eLife.

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Heavy drinking during youth can disrupt brain development

Excessive alcohol use during adolescence can disrupt the development of brain and increase risk of substance use disorder later in life, a study says.

“The maturation of the brain is still ongoing in adolescence, and especially the frontal areas and the cingulate cortex develop until the twenties. Our findings strongly indicate that heavy alcohol use may disrupt this maturation process,” said first author of the study Noora Heikkinen from University of Eastern Finland.

Cingulate cortex has an important role in impulse control, and volumetric changes in this area may play an important role in the development of a substance use disorder later in life.

The study — published in the journal Addiction — performed magnetic resonance imaging (MRI) of the brain structure on young and healthy, but heavy-drinking adults who had been heavy drinkers throughout their adolescence, as well as on age-matched light-drinking control participants. 

They participated in three cross-sectional studies conducted over the course of ten years, in 2005, 2010 and 2015. The participants were 13 to 18 years old at the onset of the study.

All participants were academically successful, and the prevalence of mental health problems did not differ between the two groups.
Although the heavy-drinking participants had used alcohol regularly for ten years, approximately six-nine units roughly once a week, none of them had a diagnosed alcohol use disorder.

MRI of the brain revealed statistically significant differences between the groups. 

Among the heavy-drinking participants, grey matter volume was decreased in the anterior cingulate cortex bilaterally as well as in the right insula.

While cingulate cortex has an important role in impulse control, structural changes in the insula, on the other hand, may reflect a reduced sensitivity to alcohol’s negative subjective effects, and in this way contribute to the development of a substance use disorder.

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