About Forgetting and Alzheimer Disease
This is a series of blog posts about the learnings and discoveries I made while studying Cognitive Psychology at the University of Berkeley, California. It will introduce you to the basic concepts of human cognition; attention, memory, categorization, semantic organization, language, problem solving and decision making.
The most common cause for dementia seems to be Alzheimer Disease and, as Professor Elizabeth Mormino from Stanford California suggested, it is triggered mostly by the congregation of two proteins in our brain; one is beta amyloid and the other one tau. How they influence each other has not been completely understood, nor do we know why some people affected by a large accumulation of these two proteins develop clinical symptoms and some do not. In any case, the two proteins can cause the degeneration of the brain, particularly in the cerebral cortex area. This leads to the symptoms characteristic to dementia.
So why do these proteins accumulate in our brain in the first place? It seems that APP (amyloid precursor protein) helps the neuron to grow and repair itself, but like other proteins it does not age well and gets at some point replaced and recycled. This recycling process for some reason is not very reliable and there are often left overs (amyloid beta) which could then bundle up into a cluster due to their sticky surface. This non-recycled waste sits in between neurons and their synapses and blocks the effective communication or signaling between them, which in return hinders the maintenance and formation of (new) neurons. From what we know about Long Term Memory – this process is important for the creation of memory codes.
On the other hand there is TAU. This protein plays its part inside the neuron where it holds together the microtubules that are important for the transportation of nutrients amongst other things. Here is where the uncertainty comes in. Researchers like Carol Colton from Duke University suggest that amyloid beta initiates a process that leads to false functioning TAU proteins. TAU starts abandoning its job and bundles up with other TAU proteins to form clusters inside the neuron. This in turn results in cell death which initiates other chain reactions. These two combined protein malfunctions, the abnormal behavior of beta amyloid and TAU, can lead to the fatal consequences we can observe in Alzheimer patients.
The first clinical symptoms that are recognizable from the outside are a less well performing short term memory (STM). Whereas apparently the hippocampus, is one of the first brain components severely damaged in Alzheimer disease and accounts for one hallmark of early Alzheimer: the difficulty of remembering recent events, without any trouble remembering events from long ago.
We know that the hippocampus is the central part of our ‘working memory’ and it’s loss immediately affects – amongst others – not only perceptual capacities of our brain, but also the ability to understand and comprehend written and spoken language. I assume that early signs of the condition show an increased inability to keep multiple meanings of ambiguous or even regular words and sentences in STM active and therefore lose the capacity to clarify context rapidly or not anymore at all. As the disease unfolds, we would later observe how patients lose the skill to form grammatically correct sentences or any sentences with meaning (Broca and Wernicke’s area affected). As the disease continues to compromise the integrity of neurons in adjoining areas, cognitive abilities will keep suffering on an ever increasing larger scale.

