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Study neuron networks to tackle Alzheimer’s

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Twenty years of research and more than US$1 billion in clinical trials have failed to yield an effective drug treatment for Alzheimer’s disease. Most neuroscientists, physicians and drug developers now agree that people at risk for the condition will need to receive medication prior to the onset of any cognitive symptoms. Yet a major obstacle to early intervention is the absence of tools that can reveal the first manifestations of insidious disease.

Until now, researchers have focused on macroscopic changes associated with disease, such as the buildup of insoluble plaques of proteins in certain areas of the brain, or on individual genes or molecular pathways that appear to be involved in disease progression.

I argue that devices operating on a ‘mesoscopic’ scale will be needed to detect earlier disruptions in brain circuitry, and to track structural and physical damage underlying Alzheimer’s symptom stable cognitive decline: techniques that measure thousands or millions of times. Examines the activity of network neurons. Although such devices have not yet been received, many existing technologies indicate that they are within reach.

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All current approaches used to diagnose Alzheimer’s are crude and unreliable. Take the classic biomarkers of disease: for example, the formation of plaques of the protein β-amyloid in a person’s cerebral cortex, or elevated levels of the tau protein and moist levels of β-amyloid in their cerebrospinal fluid. Although such markers are predictive of disease, the interval between their appearance and the onset of cognitive problems is highly variable, ranging from months to decades.

Often, people with a high density of plaques or an ominous cerebrospinal fluid reading show no signs of dementia on behavioral tests. Others show classic symptoms of the disease, such as memory loss, confusion and an inability to devise a simple plan.

More consistently associated with cognitive difficulties are neurofibrillary tangles – aggregates of tau proteins commonly found in the hippocampus and amygdala (parts of the brain involved in memory and emotion) and in the cerebral cortex. Yet this correlation is also imperfect.

And unlike amyloid plaques, which can be monitored using a scanning technique known as positron emission tomography (PET), there is no imaging procedure yet available to detect tangles in living people.

So although all of these markers may be precursors to disease, none of them capture the subtle disruptions in brain circuitry that mark the onset of cognitive decline or allow researchers to track disease progression from week to week and month to month. Enables tracking.

Nor do they reveal anything about the short-term fluctuations in cognitive ability often seen in people with Alzheimer’s. For example, relatives and caregivers often report that for some time, a person with Alzheimer’s may behave normally and be able to engage in conversation, and then an hour later able to remember this. Unable to know what just happened.

In addition to biomarkers, clinicians use a range of neuropsychological tests to diagnose Alzheimer’s disease. These test a person’s memory, emotional reactions, language skills and ability to solve problems or count. However, such tests fail to capture the subtleties of cognitive deficits at every stage of the disease.

For example, asking someone to recall a list of recently viewed objects will not reveal how well they are able to pull together memory fragments to make appropriate decisions and predictions. Similarly, being able to engage in sequentially numbered points (a standard test of executive function) goes far beyond mentally mapping out the steps needed to achieve an objective in daily life, such as eating a meal. Shopping.

Imaging issues

One of the different types of brain imaging commonly used to screen for and diagnose Alzheimer’s is functional magnetic resonance imaging (fMRI). It tracks changes in blood oxygen to the brain when a person is at rest or performing some cognitive task. The aim is to reveal faulty wiring or differences in regional brain activity that are commonly seen.

However, standard fMRI is limited to scanning 86 billion human brain neurons and several thousand times as many synapses with less than 20,000 voxels (volumetric pixels). With this technique, each tone corresponds to an arbitrary amount of tissue rather than to a specific brain network that mediates cognitive processes. PET, which assesses blood flow and metabolism, as well as the location and density of amyloid plaques, also has low spatial resolution.

Furthermore, current tools used to diagnose Alzheimer’s disease and track its progression do not account for congenital or acquired individual differences in brain structure that can significantly alter people’s tolerance to brain pathology.

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