Islamabad - Different triggers spark stroke, injuries and neurodegenerative diseases, but the molecular chain of events responsible for brain cell death in these conditions are the same. Research partners Dr Ted Dawson, PhD, now director of the Institute for Cell Engineering at the Johns Hopkins University School of Medicine, and Valina Dawson, PhD, professor of neurology, and their research group conducted experiments on laboratory-grown cells to determine the culprit in the event chain that ultimately causes cell death.

The new research builds on a growing body of knowledge of a distinct form of programmed brain cell death dubbed “parthanatos” by the team in earlier work to distinguish it from other types of cell death, such as apoptosis, necrosis, or autophagic death.

The research teams found that while stroke, injury, Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease have very different causes and symptoms, they share the brain cell death mechanism, parthanatos, and PARP, an enzyme involved in the process.

“I can’t overemphasize what an important form of cell death it is; it plays a role in almost all forms of cellular injury,” says Dr. Dawson.

The combined research groups have spent years breaking down each link in the parthanatos chain of events and tracing what roles proteins play in the process.

Previous research indicated that when a protein - mitochondrial apoptosis-inducing factor (AIF) - moves from its residing location in the energy-producing mitochondria of the cell to the nucleus, it causes the genome housed in the nucleus to be carved up, leading to cell death.

Anxiety can increase dementia risk

Upon observing that stress exacerbates mental illnesses, researchers set out to address the question of whether anxiety damages the brain and whether they could pinpoint mechanisms behind the link between stress and mental illness.

The researchers - led by Dr Linda Mah of the Rotman Research Institute at Baycrest Health Sciences conducted the research and reviewed that animal and human studies that examined brain areas affected by chronic anxiety, fear and stress.

In detail, they reviewed recent evidence from studies of stress and fear conditioning in animals, as well as neuroimaging studies of stress and anxiety in both healthy people and clinical populations.

For many of us, fear, anxiety and stress are a normal, occasional part of life; we get stressed before taking a test or going for a job interview, for example. It is when these instances of anxiety become more frequent that they interfere with daily life.

The team defines chronic stress as “a pathological state that is caused by prolonged activation of the normal acute physiological stress response,” which can then, in turn, cause problems for the immune, metabolic and cardiovascular systems.

Likewise, chronic stress can cause the brain’s hippocampus to atrophy. This brain area is important for long-term memory and spatial navigation.

Results revealed that there were similar patterns of aberrant brain activity in the wake of fear, anxiety and chronic stress. In detail, the amygdala was overactive and the PFC - which contains the “thinking areas” of the brain that regulate emotional responses - was under active.

Interestingly, over a decade ago, renowned neurologist Dr Helen Mayberg first identified what the researchers call the “see-saw relationship” between the amygdala and the PFC in a breakthrough study.

However, not all hope is lost. Dr Mah also suggests that damage to the hippocampus and PFC as a result of stress is not entirely irreversible. She notes that both anti-depressant treatment and physical activity have both shown promise in increasing hippocampal neurogenesis.