Introduction
The purpose of this essay is to examine the concepts of sleep quality and memory as well
as how sleep affects memory performance. Sleep may be crucial for repairing
neurobehavioral processes, psychosocial characteristics, and cognitive reserve. A
person who is sleep deprived cannot focus their attention adequately and so cannot learn
efficiently. Sleep plays a part in consolidation of memories, which is necessary for
learning new knowledge. The quality of sleep significantly affects the ability of an
individual to learn new motor skills and perform them. Aging can be linked to deficits in
executive function and attentional processing of information needed to solve problems,
which may be the cause of working memory impairment.
Link between memory and ageing
According to Morcom and Friston (2012), aging often results in a reduction in cognitive
function, particularly episodic memory (EM), which is the ability to recall precise event
details. Understanding this decline and the prominent individual differences that
characterise it is a major research challenge. This raises the possibility that there are
particular neural mechanisms and resources that support good function as we age. Prior
to the development of functional neuroimaging, it was believed that age-related declines
in episodic memory were simply the result of dysfunction in critical networks and regions,
particularly the medial temporal lobes (MTL) and prefrontal cortex (PFC). Indeed, this
lesion model predicts that older adults may exhibit "under-recruitment," or decreased
activity in comparison to younger adults. This may occur in bilateral rather than unilateral
prefrontal cortex activity in episodic memory.
It has long been understood that the hippocampus and other associated structures in the
medial temporal lobe (MTL) are crucial for episodic memory, but lesion studies have not
yet revealed whether the hippocampus is also crucial for later memory retrieval. This
problem can be clarified using functional magnetic resonance imaging (fMRI), as well as
specific types of positron emission tomography (PET) investigations that allow for the
distinct investigation of encoding and retrieval of brain networks. MTL regions were found
to be involved in both the formation (encoding) of new episodic memories and their
subsequent retrieval in early functional brain imaging studies. A function for MTL
, structures in episodic encoding and retrieval has been validated in recent fMRI studies
using more sophisticated methods for data gathering and processing.
One of the most common subjective concerns of older adults is episodic memory loss,
which is characterized by the encoding, storing, and retrieval of personal experiences
within their temporal and spatial contexts. According to Moutoussamy, Taconnat, Pothier,
Toussaint and Fay (2022), ineffective encoding and retrieval procedures are hampered
by an age-related decrease in processing resources. By providing environmental support,
such as specific instructions, materials, or cues, this difficulty can be reduced, improving
older adults' memory performance and even reducing the age effect. As a matter of fact,
cued recall, a memory task that offers environmental assistance, uses less executive
resources than free recall, a memory task that does not.
A perceived and risky component of human maturing is mental deterioration, including
hindered long-haul maintenance of roundabout recollections. Two prominent, albeit
distinct, signs of aging run parallel to these cognitive alterations. The first is structural
brain atrophy, which is most pronounced in the midline of the frontal lobe. The second is
decreased slow wave activity (SWA) and disrupted electroencephalographic (EEG)
quality of non-rapid eye movement (NREM) slow wave sleep (SWS). The underlying
nature of elderly deficient NREM SWA (i.e. whether age-related structural changes are
associated with disrupted sleep physiology) and whether such structural and
physiological changes are associated with age-related memory impairment remain
unknown despite these coexisting structural, physiological, and cognitive changes,
mentions (Mander, Rao, Saletin, Lindquist, Ancoli-Israel, Jagust & Walker, 2013).
In healthy young adults, an accumulating body of evidence supports a function for NREM
slow wave sleep physiology in the long-term consolidation of episodic memories. NREM
SWS, as compared to equivalent time awake, inhibits the offline erosion of episodic
memory representations across time, resulting in greater retention8. Furthermore,
electrical stimulation of the SWA over the prefrontal cortex (PFC) improves episodic
memory retention. These findings have been considered mechanistically within a
postulated hippocampal-neocortical framework of memory consolidation, in which NREM
SWS promotes the transformation of episodic representations from an initially
The purpose of this essay is to examine the concepts of sleep quality and memory as well
as how sleep affects memory performance. Sleep may be crucial for repairing
neurobehavioral processes, psychosocial characteristics, and cognitive reserve. A
person who is sleep deprived cannot focus their attention adequately and so cannot learn
efficiently. Sleep plays a part in consolidation of memories, which is necessary for
learning new knowledge. The quality of sleep significantly affects the ability of an
individual to learn new motor skills and perform them. Aging can be linked to deficits in
executive function and attentional processing of information needed to solve problems,
which may be the cause of working memory impairment.
Link between memory and ageing
According to Morcom and Friston (2012), aging often results in a reduction in cognitive
function, particularly episodic memory (EM), which is the ability to recall precise event
details. Understanding this decline and the prominent individual differences that
characterise it is a major research challenge. This raises the possibility that there are
particular neural mechanisms and resources that support good function as we age. Prior
to the development of functional neuroimaging, it was believed that age-related declines
in episodic memory were simply the result of dysfunction in critical networks and regions,
particularly the medial temporal lobes (MTL) and prefrontal cortex (PFC). Indeed, this
lesion model predicts that older adults may exhibit "under-recruitment," or decreased
activity in comparison to younger adults. This may occur in bilateral rather than unilateral
prefrontal cortex activity in episodic memory.
It has long been understood that the hippocampus and other associated structures in the
medial temporal lobe (MTL) are crucial for episodic memory, but lesion studies have not
yet revealed whether the hippocampus is also crucial for later memory retrieval. This
problem can be clarified using functional magnetic resonance imaging (fMRI), as well as
specific types of positron emission tomography (PET) investigations that allow for the
distinct investigation of encoding and retrieval of brain networks. MTL regions were found
to be involved in both the formation (encoding) of new episodic memories and their
subsequent retrieval in early functional brain imaging studies. A function for MTL
, structures in episodic encoding and retrieval has been validated in recent fMRI studies
using more sophisticated methods for data gathering and processing.
One of the most common subjective concerns of older adults is episodic memory loss,
which is characterized by the encoding, storing, and retrieval of personal experiences
within their temporal and spatial contexts. According to Moutoussamy, Taconnat, Pothier,
Toussaint and Fay (2022), ineffective encoding and retrieval procedures are hampered
by an age-related decrease in processing resources. By providing environmental support,
such as specific instructions, materials, or cues, this difficulty can be reduced, improving
older adults' memory performance and even reducing the age effect. As a matter of fact,
cued recall, a memory task that offers environmental assistance, uses less executive
resources than free recall, a memory task that does not.
A perceived and risky component of human maturing is mental deterioration, including
hindered long-haul maintenance of roundabout recollections. Two prominent, albeit
distinct, signs of aging run parallel to these cognitive alterations. The first is structural
brain atrophy, which is most pronounced in the midline of the frontal lobe. The second is
decreased slow wave activity (SWA) and disrupted electroencephalographic (EEG)
quality of non-rapid eye movement (NREM) slow wave sleep (SWS). The underlying
nature of elderly deficient NREM SWA (i.e. whether age-related structural changes are
associated with disrupted sleep physiology) and whether such structural and
physiological changes are associated with age-related memory impairment remain
unknown despite these coexisting structural, physiological, and cognitive changes,
mentions (Mander, Rao, Saletin, Lindquist, Ancoli-Israel, Jagust & Walker, 2013).
In healthy young adults, an accumulating body of evidence supports a function for NREM
slow wave sleep physiology in the long-term consolidation of episodic memories. NREM
SWS, as compared to equivalent time awake, inhibits the offline erosion of episodic
memory representations across time, resulting in greater retention8. Furthermore,
electrical stimulation of the SWA over the prefrontal cortex (PFC) improves episodic
memory retention. These findings have been considered mechanistically within a
postulated hippocampal-neocortical framework of memory consolidation, in which NREM
SWS promotes the transformation of episodic representations from an initially
