Dementia Treatment and Prevention Notes | EduRev

: Dementia Treatment and Prevention Notes | EduRev

 Page 1


1
Dementia Treatment and 
Prevention 
Maria T. Caserta, MD, PhD
Director of Geriatric Psychiatry
Dept. of Psychiatry and Behavioral Medicine 
USF
Dementia
• Dementia is a major public health concern 
– Prevalence
– Chronicity
– Caregiver burden
– Financial costs
There are no cures for the neurodegenerative 
dementias.
Page 2


1
Dementia Treatment and 
Prevention 
Maria T. Caserta, MD, PhD
Director of Geriatric Psychiatry
Dept. of Psychiatry and Behavioral Medicine 
USF
Dementia
• Dementia is a major public health concern 
– Prevalence
– Chronicity
– Caregiver burden
– Financial costs
There are no cures for the neurodegenerative 
dementias.
2
Alzheimer brain - microscopic
The hallmarks of 
Alzheimer's pathology are 
amyloid plaques and 
neurofibrillary tangles, 
both of which are 
visualized here with 
thioflavin-S labeling. 
Neurofibrillary tangles are 
seen here as "flame-
shaped" structures, and 
often fill the neuronal cell 
body which they occupy. 
Amyloid plaques are seen 
as diffuse and round 
fibrous structures.
From the Basic Human Brain 
Research  Laboratory at 
Northwestern University’s 
Alzheimer’s disease Center:
http://www.brain.nwu.edu/galle
ry/P&Tpicture.htm
Page 3


1
Dementia Treatment and 
Prevention 
Maria T. Caserta, MD, PhD
Director of Geriatric Psychiatry
Dept. of Psychiatry and Behavioral Medicine 
USF
Dementia
• Dementia is a major public health concern 
– Prevalence
– Chronicity
– Caregiver burden
– Financial costs
There are no cures for the neurodegenerative 
dementias.
2
Alzheimer brain - microscopic
The hallmarks of 
Alzheimer's pathology are 
amyloid plaques and 
neurofibrillary tangles, 
both of which are 
visualized here with 
thioflavin-S labeling. 
Neurofibrillary tangles are 
seen here as "flame-
shaped" structures, and 
often fill the neuronal cell 
body which they occupy. 
Amyloid plaques are seen 
as diffuse and round 
fibrous structures.
From the Basic Human Brain 
Research  Laboratory at 
Northwestern University’s 
Alzheimer’s disease Center:
http://www.brain.nwu.edu/galle
ry/P&Tpicture.htm
3
Course of Aging, MCI and AD
AAMI / ARCD
MCI
Clinical 
AD
Time (Years)
Cognitive Decline
“Brain
”AD
Brain 
Aging Mild
Moderate
Moderately
Severe
Severe
(Ferris, 4/03)
Brain Aging
Possible Treatment Outcomes
Function
Time
Treatment
Disease arrest
Slowed 
progression
Symptomatic 
benefit
No benefit
Page 4


1
Dementia Treatment and 
Prevention 
Maria T. Caserta, MD, PhD
Director of Geriatric Psychiatry
Dept. of Psychiatry and Behavioral Medicine 
USF
Dementia
• Dementia is a major public health concern 
– Prevalence
– Chronicity
– Caregiver burden
– Financial costs
There are no cures for the neurodegenerative 
dementias.
2
Alzheimer brain - microscopic
The hallmarks of 
Alzheimer's pathology are 
amyloid plaques and 
neurofibrillary tangles, 
both of which are 
visualized here with 
thioflavin-S labeling. 
Neurofibrillary tangles are 
seen here as "flame-
shaped" structures, and 
often fill the neuronal cell 
body which they occupy. 
Amyloid plaques are seen 
as diffuse and round 
fibrous structures.
From the Basic Human Brain 
Research  Laboratory at 
Northwestern University’s 
Alzheimer’s disease Center:
http://www.brain.nwu.edu/galle
ry/P&Tpicture.htm
3
Course of Aging, MCI and AD
AAMI / ARCD
MCI
Clinical 
AD
Time (Years)
Cognitive Decline
“Brain
”AD
Brain 
Aging Mild
Moderate
Moderately
Severe
Severe
(Ferris, 4/03)
Brain Aging
Possible Treatment Outcomes
Function
Time
Treatment
Disease arrest
Slowed 
progression
Symptomatic 
benefit
No benefit
4
Dementia
• Clinicians prescribe various 
pharmacotherapies to alleviate symptoms 
and delay disease.
• Currently 5 drugs have FDA approval for 
treating and  managing dementias.
Therapeutic approaches based on 
pathogenic mechanism
• Cholinergic deficiency 
• 1st generation:
• 2nd generation:
• Cholinesterase 
inhibitors:
• Tacrine
• Donepezil
• Galantamine
• Rivastigmine
Page 5


1
Dementia Treatment and 
Prevention 
Maria T. Caserta, MD, PhD
Director of Geriatric Psychiatry
Dept. of Psychiatry and Behavioral Medicine 
USF
Dementia
• Dementia is a major public health concern 
– Prevalence
– Chronicity
– Caregiver burden
– Financial costs
There are no cures for the neurodegenerative 
dementias.
2
Alzheimer brain - microscopic
The hallmarks of 
Alzheimer's pathology are 
amyloid plaques and 
neurofibrillary tangles, 
both of which are 
visualized here with 
thioflavin-S labeling. 
Neurofibrillary tangles are 
seen here as "flame-
shaped" structures, and 
often fill the neuronal cell 
body which they occupy. 
Amyloid plaques are seen 
as diffuse and round 
fibrous structures.
From the Basic Human Brain 
Research  Laboratory at 
Northwestern University’s 
Alzheimer’s disease Center:
http://www.brain.nwu.edu/galle
ry/P&Tpicture.htm
3
Course of Aging, MCI and AD
AAMI / ARCD
MCI
Clinical 
AD
Time (Years)
Cognitive Decline
“Brain
”AD
Brain 
Aging Mild
Moderate
Moderately
Severe
Severe
(Ferris, 4/03)
Brain Aging
Possible Treatment Outcomes
Function
Time
Treatment
Disease arrest
Slowed 
progression
Symptomatic 
benefit
No benefit
4
Dementia
• Clinicians prescribe various 
pharmacotherapies to alleviate symptoms 
and delay disease.
• Currently 5 drugs have FDA approval for 
treating and  managing dementias.
Therapeutic approaches based on 
pathogenic mechanism
• Cholinergic deficiency 
• 1st generation:
• 2nd generation:
• Cholinesterase 
inhibitors:
• Tacrine
• Donepezil
• Galantamine
• Rivastigmine
5
Correlation of cognitive function 
with cholinergic dysfunction
Comparison of 
11
C-nicotine uptake as assessed by PET and the MMSE
1
1
Reprinted with permission from Nordberg A. Biological markers and the cholinergic hypothesis 
in Alzheimer's disease. Acta Neurol Scand Suppl. 1992;139:54-8. PMID: 1414270
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1414270&form=6&db=m&Dopt=b
(S)(-)-
11
C-nicotine uptake
nCi/cm
3
/dose bw
-1
Normal cholinergic function*
*Adapted with permission from Adem A. Putative mechanisms of action of tacrine in 
Alzheimer's disease. Acta Neurol Scand Suppl. 1992;139:69-74. PMID: 1384265
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=1384265&form=6&db=m&Dopt=b
Acetyl CoA
+ Choline
Ach
Ach
ChAT
Presynaptic neuron
Choline
Choline
+ Acetate
Acetylcholinesterase
Cholinergic receptor
Postsynaptic neuron
Synaptic cleft
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