How does long term memory and short term memory differ in people with Alzheimer?

Running head: NEUROPSYCHOLOGY
How does long term memory and short term memory differ in people with Alzheimer?
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NEUROPSYCHOLOGY
Alzheimer’s Disease
Alzheimer’s is an irreversible, polygenetic neurodegenerative disorder of the brain
that slowly destroys the thinking and the memory skills and eventually hampers the ability to
carry out simple tasks to sustain activities of daily living. The symptoms of Alzheimer’s
disease (AD) first appear after 65 years of age. AD is also regarded as one of the most
common cause of dementia among the older adults. In dementia there occurs loss of cognitive
functioning like remembering, thinking and logical reasoning along with problem in
executing normal behavioural abilities (Bloom, 2014).
Pathophysiology of AD
The change or the damage in brain of individuals with AD starts a decade before the
problems like memory loss and cognition loss surfaces. The changes in the AD mainly occur
in the nerve cells of the brain. Brain has approximately 100 billion nerve cells (neurons).
Each nerve connects with the other in order to form interconnected networks of neurons. The
onset of the AD takes place by the formation and subsequent deposition of the bet-amyloid
protein known as senile plaques and twisted tangles of protein know as tau proteins in
between the spaces of the nerve cells (Bloom, 2014). The deposition of the beta-amyloid
protein in between the spaces of the nerve cell networks hamper propagation of the neuronal
impulses through the nerve endings (synapse) and thereby hamper the normal functioning of
the nerve leading to eventual aopotsis of the nerve cells. The amyloid proteins surround with
dead nerve cells look like plaques. Amyloid plaques are made of amyloid fibrils named after
beta amyloid peptides. Beta amyloid peptide (A-beta) is a 770 segment residue of the
transmembrane protein amyloid beta precursor protein (beta-PP) which is 1770 aminio acid
long (Šimić et al., 2016). Beta amyloid protein is excised from beta-PP by the action of the
two membrane anchored proteolytic enzyme known as beta and gama secretase. However,

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NEUROPSYCHOLOGY
certain mutation in the beta and the gamma precursor enzymes results in faulty excision of
the Abeta –from the beta-PP (42 amino acid residue protein is generated instead of 770 amino
acid long) leading to misfolding and subsequent insolubility of the protein. Amyloid plaques
are initially soluble proteins but misfolding of the protein during the post-translational
modifications hampers protein solubility leading to extracellular deposition of the protein in
between the nerve spaces (Spires-Jones & Hyman, 2014).
Tau is a microtubule associated protein and that is sorted in the neuronal axons in the
normal physiological conditions. In AD, the mechanism of tau sorting fails and tau becomes
missorted into somato-dendritic compartment. The aberrant amyloid-beta production is found
responsible for tau missorting. The physiological axonal sorting of Tau mainly depends on
the developmental stage of the neurons and the phosphorylation of Tau and microtubule
cytoskeleton. In disease associated sorting of Tau during AD, leads to increased
phosphorylation of Tau hampers microtubule interactions. This in turn hampers the axonal
sorting leading to its aggregation in the tau and subsequent formation of prion proteins and
deposition in between the nerve ending and leading towards disease propagation (Zempel &
Mandelkow, 2014).
Short term and long-term memory
AD starts with complain about the memory loss that affect episodic memory, speech
problems along with problem in visual orientation and semantic problems. Memory is
defined as a process of sorting, encoding and retrieving information about the inner and outer
stimuli and presentation of the retrieved information in the nervous system so that it can be
used or retrieved. Different types of memories have been identified to which different
neuroanatomical and neurophysiological functions correlates: short-term and long-term
memory and sensory memory (Jahn, 2013). Sensory memory lasts for milli seconds to