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Antidepressant could help slow Alzheimer’s

Researchers have found that a commonly prescribed antidepressant can reduce production of the main ingredient in Alzheimer’s brain plaques.

Researchers at Washington University School of Medicine in St. Louis and the
University of Pennsylvania, support preliminary mouse studies that evaluated a variety of
antidepressants.

Brain plaques are tied closely to memory problems and other cognitive impairments caused by Alzheimer’s disease.

Stopping plaque buildup may halt the disastrous mental decline caused by the disorder.

The scientists found that the antidepressant citalopram stopped the growth of plaques in a mouse model of Alzheimer’s disease. And in young adults who were cognitively healthy, a single dose of the antidepressant lowered by 37 percent the production of amyloid beta, the primary ingredient in plaques.

Senior author John Cirrito, PhD, assistant professor of neurology at Washington University, said antidepressants appear to be significantly reducing amyloid beta production, and that’s exciting.

He said while antidepressants generally are well tolerated, they have risks and side effects. Until we can more definitively prove that these drugs help slow or stop Alzheimer’s in humans, the risks aren’t worth it. There is still much more work to do.

Amyloid beta is a protein produced by normal brain activity.

Levels of this protein rise in the brains of patients with Alzheimer’s, causing it to clump together into plaques.

Plaques also are sometimes present in cognitively normal brains.

Prolonged workouts can be detrimental to heart health

Studies have revealed that overdoing vigorous exercise can lead to risks of major health issues even death.

A German and a Swedish study has pointed out that the intensity and duration of exercise are critical factors to determine person’s physical health.

They also stated that a similar U-shaped or reverse J-shaped curve pattern for the dose responses to the effect of exercise and maximum cardiovascular benefits are achieved if performed at moderate doses.

Existing facts propose that heart disease patients should do up to an hour of moderate intensity aerobic activity at least five times a week.
The study also suggested that genes may also play a crucial role in determining health safety limits and that there is a thin line that separates the accurate information and pointless alarmism leading to inactivity and following heart disease.
However, it was concluded that benefits of exercise are definitely unquestionable and that it needs to be reinforced but the further study on the subject is required to obtain results on how to achieve maximum benefits from exercise by averting undesirable health risks.

How ‘deadly’ cone snail venom helps cut chronic pain

Researchers have shown how the toxin Vc1.1 inhibits neuronal calcium channels to reduce neuropathic pain.

The venom from marine cone snails, used to immobilize prey, contains numerous peptides called conotoxins, some of which can act as painkillers in mammals.

The findings help explain the analgesic powers of this naturally occurring toxin and could eventually lead to the development of synthetic forms of Vc1.1 to treat certain types of neuropathic pain in humans.

Neuropathic pain, a form of chronic pain that occurs in conjunction with injury to—or dysfunction of—the nervous system, can be debilitating and difficult to treat, and the medical community is eager to find better methods to minimize what can be a serious condition.

Neuropathic pain is associated with changes in the transmission of signals between neurons, a process that depends on several types of voltage-gated calcium channels (VGCCs).

However, given the importance of these VGCCs in mediating normal neurotransmission, using them as a pharmacological target against neuropathic pain could potentially lead to undesirable side effects.

In previous studies, David Adams and colleagues from RMIT University in Melbourne showed that Vc1.1 also acts through GABAB receptors to inhibit a second, mysterious class of neuronal VGCCs that have been implicated in pain signaling but have not been well understood—R-type (Cav2.3) channels.

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