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Summary Chapter 4
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Chapter 4 lecture notes Erik Scherder
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Summary chapter 4 and lecturenotes
Aging of the world’s populaton is the ost i portant de ographic change of the previous century
and therefore a growing interest in the aging populaton arose within science.
The nor al cognitve aging process of the brain is characterized by a selectve degeneraton process.
The degeneraton process reveals itself in atrophy of the frontal and te poral lobes and in the
a ygdala-hippoca pal region. Atrophy is higher in the posterior frontal lobe than in the te poral
lobe, because there is ore white ater. Aging ainly afects white ater. The prefrontal
associaton areas are ore vulnerable for the aging process than pri ary so atosensory and visual
cortces, for the sa e reason. The aging brain has several pathological co ponents that ay
negatvely afect cell etabolis !
- Argyrophilic grains intracellular protein aggregates presented as intraneuronal lesions.
They hinder the nor al functon of tau. They occur pri arily in the neuropil.
- Lipofuscin co posed of protein and lipid, occurs in hippoca pus a ong others.
- Neuro elanin contains lipofuscin but also produces it. Occurs pri arily in the substanta
nigra and locus coeruleus, increases throughout life.
- Corpora a ylacea cytoplas atc, glycoproteina-cous inclusions, can be observed as
astrocytes. Are found in the BG, hippoca pus and spinal cord a ong other regions. In case
of AD the nu ber of corpora a ylacea shows a huge increase.
Neuritc plaques and neurofbrillary tangles are characteristc for patents with AD, but also occur in
the nor al aging process. There is li ited neuronal loss in hippoca pus, the cerebellu and in brain
ste areas. Degeneraton of the PFC during aging can also be atributed to an age-related decline in
several neurotrans iter syste s. Cholinergic syste degeneraton in basal forebrain;
noradrenergic syste neuronal loss in brainste at locus coeruleus, eaning less noradrenalin in
higher levels connected to the locus coeruleus; serotonergic syste neuronal loss in the dorsal
raphe nucleus, less serotonergic neurons in neocortex, hippoca pus and part of BG. Also the
dopa inergic syste is afected by the aging process.
The defcit in the NBM/cholinergic syste ay negatvely influence the vascularizaton of the brain
during aging. A decrease in the nicotnic-receptor actvity ay reduce the cerebral blood flow
(pressure) in the frontal and parietal lobe by a decrease in neuronal vasodilataton ( ore
vasoconstricton). Focal electrical st ulaton of the NBM can increase the cortcal cerebral blood
flow. The decline in cortcal blood flow ay only be visible fro age s0 on and/or in those with AD.
The risk for cardiovascular diseases is uch higher in older people due to less elastc veins and years
of cholesterol deposit. CV diseases partcularly tend to influence the white ater in the brain due to
decreased vascularizaton.
The accu ulaton of white ater lesions during aging starts to afect the functoning of the ARAS,
thus global cortcal arousal. At brainste level we see neuronal loss in the LC. The resultng levels of
noradrenalin delivered to higher level areas connected to the LC decline as well. A decline in
noradrenalin is observed in NBM, BG, frontote poral cortex and the hippoca pus, but not the
a ygdala. The aging process ay also afect the co unicaton of the dorsal raphe nucleus (DRN)
and serotonergic neurons, which in turn afects the neocortex, hippoca pus, and BG.
Areas that play an i portant role in EF all tend to be vulnerable to aging! Most atrophy appears to
occur in the striatu (frontostriatal circuit, i portant for episodic e ory) and the cerebellu
(frontocerebellar circuit, i portant for EF and processing speed). Si ilar degeneraton is seen in the
PFC and prefrontal white ater. Apparently, not the co plete PFC is afected, the OFC for exa ple
is often preserved. The DLPFC appears to be partcularly vulnerable to the aging process. A ong
, te poral lobe brain areas, the hippoca pus is ost afected by the aging process. The entorhinal
cortex (co unicaton between hippoca pus and PFC) appears to be less afected. Hippoca pal
atrophy ay be caused by a decrease in nerve growth factors (neurotrophin). Neurotrophins play a
ajor role in the develop ent of the hippoca pus.
Various fronto-subcortcal circuits that are involved in either cogniton or otor actvity appear to be
so close to each other that cognitve and otor disturbances are likely to occur together. Lesions
within the frontostriatal circuit can for exa ple also result in declines in otor actvity.
Actvity of the nigrostriatal/dopa inergic syste shows an age efect but is only visible in sy pto s
when the reducton in dopa inergic input is signifcant. This appears to beco e present in later
stages of aging.
White ater lesions due to aging especially occur in the frontal area, because of higher quantty of
white ater. White ater lesions are also often the result of proble s in the s all blood vessels,
based upon CV risk factors (diabetes, hypertension, age). The nature of white ater lesions is
i portant with respect to cognitve functoning. Subjectve cognitve co plaints tend to appear ore
in cases of disorders of the periventricular (around ventricular) white ater. Subjectve cognitve
co plaints ay be a predictor for developing de enta at a later o ent. Those who experienced a
progressive decline in cognitve functoning tend to show an increase in the quantty of white ater
lesions. The quantty of periventricular white mater lesions appears to be associated with the
progression of cognitve decline. Could be because the vascularizaton of the periventricular white
ater is ore sensitve to age-related neuropathology (seen in for exa ple atherosclerosis). White
ater lesions need to be present in certain quantty before they are afectng cognitve functoning.
In old-old populatons, the white ater lesions have litle/no efect on cognitve functoning, aybe
because the brain had t e to prepare and co pensate for these changes. Also no associaton was
found between EF and ‘frontal’ white ater lesions.
To conclude! especially the PFC, ACC, hippoca pus, striatu , brain ste areas and cerebellu
appear to be afected by the nor al aging process, EC less severely. These structures are i portant
in several circuits that contribute to EF and episodic e ory. Especially periventricular white ater
lesions appear to influence cognitve functoning negatvely. Regarding the ARAS, we see
degeneraton in the PFC, NBM, DRN and LC. 3 circuits are ost vulnerable! the frontocerebellar
circuit, the frontostriatal circuit and the frontohippoca pal circuit. Lesions in any of the structures
within a circuit disrupt the signal trans ission necessary for efectve co unicaton within the
circuit and between regions.
Cognitve decline in aging
EF
A decline in the PFC functoning expresses itself in i pair ent of divided atenton, set-shifting, and
inhibiton. A decline in the functoning of the striatu expresses itself as difcultes with divided
atenton across tasks of ultple sensory odalites, but also during perfor ance of a otor task
especially in co binaton with a detecton of sensory signals task. I pair ents in inhibiton are also
possible with lesions in the striatu . A decrease in EF ay depend on the extent to which white
ater lesions occur. The PFC is ost sensitve for white ater lesions.
Memory decline
Especially episodic e ory shows a decline in the aging process. Verbal episodic e ory is ost
vulnerable, because a word yields less additonal infor aton that ay contribute to encoding. There
is a progressive decline in perfor ance of episodic e ory with task difculty. An explanaton is that
older people have proble s in for ing new relatonships between words to be re e bered and the
context in which the words are presented. Wo en are beter in e orizing ite ized lists such as
groceries and na es. Talking about recogniton e ory, the explicit contextual recogniton e ory
is worse in older people. The i plicit recogniton, based on fa iliarity with the ite , is often not very
afected. I plicit recogniton ay serve as a co pensator echanis for the loss of explicit
recogniton. The hippoca pus is i portant for learning new infor aton and for retrieving
infor aton fro e ory, both visuospatal and non-visuospatal. The hippoca pus is sensitve for
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