Currently, more than 46 million people worldwide and 850,000 people in the UK are living with dementia and Alzheimer's disease, a number that is expected to double every 20 years  (Alzheimer's Disease International, www.alz.co.uk). Despite many efforts to find new disease-modifying therapies for this disease, recent clinical trials have failed to show significant benefits and currently patients are only treated with drugs that alleviate disease symptoms. Traditionally, drug discovery strategies have focused on neurons as the main targets in Alzheimer's and other brain disorders. However, in the brain there are two types of cells: nerve cells and glial cells.

 

Nerve cells or neurons pass chemical messages to each other through synapses and are essential for all brain activities such as learning, memory or movement control. In neurodegenerative diseases, such as in Alzheimer’s disease, synapses become dysfunctional and neurons eventually die causing memory deficits or learning disabilities, among other consequences.

 

Glial cells received their name from the Greek “glue”, as they hold neurons together. While for many years their importance remained unclear, we now know that they are essential for brain function: some glial cells protect the brain from infections, others insulate neuron projections with myelin, while others, called astrocytes, are in charge of feeding the neurons, protecting them from injury or helping them in synapse performance. Several studies support the idea that, while astrocytes are protective, their response may become deleterious when damage in the brain is prolonged, such as happens in Alzheimer’s disease.

 

Alzheimer’s disease is characterized by the formation of amyloid plaques in the space between brain cells and of tau tangles inside nerve cells. This abnormal accumulation or “clumps” of amyloid and tau occurs parallel with the death of nerve cells and the severity of dementia. The formation of such “clumps” is found not only in Alzheimer’s disease, but also in other neurodegenerative disorders such as Parkinson’s, Huntington’s and prion diseases. For this reason, we and other researchers are working toward finding novel ways of preventing these protein accumulations. Chaperones help the brain to get rid of abnormal protein accumulations by binding to other proteins and stopping them from clumping together and accumulating. Therefore, having more chaperones in neurons helps to stop the progression of neurodegenerative diseases.

 

The lab investigates how astrocytes, the most abundant type of glial cell, can protect nerve cells in Alzheimer's disease and how chaperones can participate in the protection exerted by astrocytes. If we are able to identify which are the factors produced by astrocytes that mediate neuroprotection, we will be able to design effective therapeutic tools.

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