Summary Chapter 5 + lecture
notes
MCI
A Mild Cognitive Impairmenti (MCI) is a noticeable cognitiie ecline, greater than the normal aging
process but not seiere enough to afect aily functioning. Preialence of MCI in ol er persons is
aroun the 5%. Some with MCI eielop AD, but not all! Some people with MCI can improie again. 2
types: (1) amnestic MCI, who are more likely to continue eieloping AD; (2) multii omain MCI. MCI
patients that show a ecline in IADL ten to haie higher risk of eieloping AD. Riisk factors associate
with MCI inclu e age, low e ucation, an the presence of Apolipoprotein E4 (iniolie in lipi
metabolism).
MCI patients ten to show focal re uction in the hippocampal iolume. oweier, global brain
atrophy in these patients is not worse than in people without ementia. Atrophy of the hippocampus
is characteristic for the amnesticiMCI type. Furthermore we see atrophy of the posterior region of
the corpus callosum an hypoperfusion of the inferior right parietal lobe.
In patients with MCI there is an eleiate leiel of neuritic plaques in the frontal, parietal, an
temporal neocortical region, an in the amyg ala. The parietal neocortical region an ientrome ial
temporal lobe structures ten to haie a higher leiel of neurofbrillary tangles. Many brain areas are
thus afecte in MCI.
ADirelate neuropathology such as the neurofbrillary tangles afects the basal forebrain/cholinergic
system in MCI as well. This cholinergic amage woul in particular amage hippocampal function
(episo ic memory).
MCI patients who eielop AD aferwar s ten to show a re uce bloo fow in seieral brain areas in
parietal an temporal lobes.
No stu y about brain stem areas of ARiAS an the relationship with MCI. oweier, you woul expect
that areas goierning the leiels of global arousal (such as L C an DRiN) woul show changes in
function uring the course of MCI.
The iulnerability of functional circuitry to egeneration is exacerbate in MCI. Especially the
hippocampus woul be more afecte than in the normal aging process. Also more pronounce
egeneration was foun in the PFC an ACC. This implies that frontohippocampal an frontostriatal
circuits are sensitiie to egeneration in MCI, although this relationship has not been iniestigate yet.
Atrophy of ACC is characteristic for MCI patients who later eielop AD. MCI patients that remain
clinically stable ten to haie a high preialence of periientricular white mater lesions (not those that
progress into AD!!!). Seieral brain areas are more iulnerable for accumulation of neuropathological
features as plaques an tangles: PFC, ACC an hippocampus are most iulnerable.
Symptiomatiology
Executiie ysfunction becomes more pronounce in MCI patients compare to healthy el erly.
Especially the egeneration of hippocampus is responsible; interrupts functional relationship
between hippocampus, PFC an parietal cortex. Impairment in more than one cognitiie function is
characteristic for MCI. Ofen a more pronounce efcit is seen in planning, iii e atention, seti
shifing, an inhibition. Furthermore, EF, episo ic memory an spee of information processing ten
to eteriorate faster than in normal aging. In the transitional stage from MCI to AD, there is the
characteristic relationship between impairment in episo ic memory an amage to the me ial
temporal lobe, in particular the hippocampus. Delaye recall of wor lists learne before ma e the
best istinction between ol er persons without cognitiie impairment an those in a preclinical stage
of AD (which is, MCI). Also Trailmaking B will istinguish between the two groups.
notes
MCI
A Mild Cognitive Impairmenti (MCI) is a noticeable cognitiie ecline, greater than the normal aging
process but not seiere enough to afect aily functioning. Preialence of MCI in ol er persons is
aroun the 5%. Some with MCI eielop AD, but not all! Some people with MCI can improie again. 2
types: (1) amnestic MCI, who are more likely to continue eieloping AD; (2) multii omain MCI. MCI
patients that show a ecline in IADL ten to haie higher risk of eieloping AD. Riisk factors associate
with MCI inclu e age, low e ucation, an the presence of Apolipoprotein E4 (iniolie in lipi
metabolism).
MCI patients ten to show focal re uction in the hippocampal iolume. oweier, global brain
atrophy in these patients is not worse than in people without ementia. Atrophy of the hippocampus
is characteristic for the amnesticiMCI type. Furthermore we see atrophy of the posterior region of
the corpus callosum an hypoperfusion of the inferior right parietal lobe.
In patients with MCI there is an eleiate leiel of neuritic plaques in the frontal, parietal, an
temporal neocortical region, an in the amyg ala. The parietal neocortical region an ientrome ial
temporal lobe structures ten to haie a higher leiel of neurofbrillary tangles. Many brain areas are
thus afecte in MCI.
ADirelate neuropathology such as the neurofbrillary tangles afects the basal forebrain/cholinergic
system in MCI as well. This cholinergic amage woul in particular amage hippocampal function
(episo ic memory).
MCI patients who eielop AD aferwar s ten to show a re uce bloo fow in seieral brain areas in
parietal an temporal lobes.
No stu y about brain stem areas of ARiAS an the relationship with MCI. oweier, you woul expect
that areas goierning the leiels of global arousal (such as L C an DRiN) woul show changes in
function uring the course of MCI.
The iulnerability of functional circuitry to egeneration is exacerbate in MCI. Especially the
hippocampus woul be more afecte than in the normal aging process. Also more pronounce
egeneration was foun in the PFC an ACC. This implies that frontohippocampal an frontostriatal
circuits are sensitiie to egeneration in MCI, although this relationship has not been iniestigate yet.
Atrophy of ACC is characteristic for MCI patients who later eielop AD. MCI patients that remain
clinically stable ten to haie a high preialence of periientricular white mater lesions (not those that
progress into AD!!!). Seieral brain areas are more iulnerable for accumulation of neuropathological
features as plaques an tangles: PFC, ACC an hippocampus are most iulnerable.
Symptiomatiology
Executiie ysfunction becomes more pronounce in MCI patients compare to healthy el erly.
Especially the egeneration of hippocampus is responsible; interrupts functional relationship
between hippocampus, PFC an parietal cortex. Impairment in more than one cognitiie function is
characteristic for MCI. Ofen a more pronounce efcit is seen in planning, iii e atention, seti
shifing, an inhibition. Furthermore, EF, episo ic memory an spee of information processing ten
to eteriorate faster than in normal aging. In the transitional stage from MCI to AD, there is the
characteristic relationship between impairment in episo ic memory an amage to the me ial
temporal lobe, in particular the hippocampus. Delaye recall of wor lists learne before ma e the
best istinction between ol er persons without cognitiie impairment an those in a preclinical stage
of AD (which is, MCI). Also Trailmaking B will istinguish between the two groups.
