A protein in your brain can be your weapon against Alzheimer’s disease

Researchers have found that a protein that regulates white blood cells in the human brain could protect against Alzheimer’s disease.

The results  suggest that this protein, called CD33, could have important implications in the fight against Alzheimer’s disease.

“Immune cells in the brain, called microglia, play a critical role in Alzheimer’s disease,” explained  co-author of the study.

“They can be harmful or protective. Swaying microglia from a harmful to protective state could be the key to treating the disease,” the author added. Scientists have identified the CD33 protein as a factor that may decrease a person’s likelihood of this disease.

Now, this research has shown that the most common type of CD33 protein plays a crucial role in modulating the function of microglia. “The fact that CD33 is found on microglia suggests that immune cells can protect the brain from Alzheimer’s disease under the right circumstances,” said the  first author of the study.

Alzheimer’s disease affects more than 44 million people around the world. “These findings set the stage for future testing of a causal relationship between CD33 and Alzheimer’s Disease, as well as testing therapeutic strategies to sway microglia from harmful to protecting against the disease – by targeting CD33,” said the researcher.

“Microglia have the potential to ‘clean up’ the neurodegenerative plaques, through a process called phagocytosis — so a therapy to harness this ability to slow down or reverse this mental health disorder can be envisioned,” he said.


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New method found to inhibit Parkinson’s disease

Contrary to earlier discovery that a chemical found in a synthetic opioid, MPTP, induced a form of Parkinson's disease, a new study has found that it is an enzyme in the body that can metabolise compounds formed in the brain from alkaloids causing a neurodegenerative condition in mice.

The study  suggested that the enzyme, mitochondrial CYP2D6, presents a potentially powerful new target for Parkinson's treatment. "Over the past two or three decades, researchers have tried inhibiting the process by they believed MPTP was metabolised, with mixed success," he said.

"We believe that mitochondrial CYP2D6 is the more direct drug target, which might prove better in treating idiopathic Parkinson's disease," added one of the researchers. The study investigated the mechanism of Parkinson's disease when a specific cause cannot be pinpointed.

Previous studies have shown that MPTP and similar toxic compounds induce Parkinson's disease in rodents and primates. The mechanism of action, as scientists understood it, involved the compounds being oxidised to form MPP+, a toxic metabolite.

The enzyme that was believed to be responsible is called monoamine oxidase B (MAO-B), present in the nervous system's glial cells. In that conception of the mechanism, MPP+ was thought to then be transferred to dopamine neurons by dopamine transporter proteins, and, indeed, Parkinson's is characterised by unusually low dopamine levels in the brain.

Researchers have tried to stem the effects of Parkinson's by targeting two players in this presumed pathway, both MAO-B and the dopamine transporter protein, with only mixed success. In earlier work, Avadhani and colleagues had shown that the enzyme CYP2D6, localised to the body's energy factories, the mitochondria, could play a role in metabolising MPTP to MPP+.

In the new investigation, they took a closer look at beta-carbolines and isoquinolines, toxins that resemble MPTP which the body produces from substances found in tobacco smoke, alcohol, and some foods.

They found that, instead of MAO-B, it was mitochondrial CYP2D6 that activate the beta-carbolines and isoquinolines inside the dopamine-producing neurons, rather than the glial cells. This route of activation, in a mouse model, results in neuronal damage and oxidative stress, symptoms akin to Parkinson's. "CYP2D6 is known to play a role in influencing the activity of a number of drugs," said a researcher.

In an attempt to target this pathway, the researchers showed that mice lacking CYP2D6 did not exhibit severe symptoms than mice with the protein did. In addition, an inhibitor of CYP2D6 prevented neuronal damage in the mice.

"The CYP2D6 inhibitor ajmalicine is a member of the reserpine family of alkaloids, found in the plant Rauwolfia serpentine and was long used in India for treating mental illness, such as paranoia and schizophrenia," he said. "Mitochondrial targeting of such compounds is likely to be effective in treating Parkinson's patients, and pursuing that is our future strategy," said the researcher.

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