Geropsychology and

Alzheimers Disease
Psychology 2230
April 21, 2016

Anderson D. Smith
Regents Professor of Psychology Emeritus
anderson.smith@carnegie.gatech.edu

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Geropsychology
Geropsychology is one of 15 specialties
in professional psychology defined by the
American Psychological Association
(APA)
A specialty is an APA defined area of
psychological practice which requires
advanced knowledge and skills acquired
through an organized sequence of
education and training.
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Geropsychology
Organized education and training
Adult development and aging: normal aging-related biological,
psychological, social change and sociocultural factors (e.g.,
gender, ethnicity)
Behavioral and mental health in late life: medical illnesses,
psychopathology, neuroscience, and functional changes
Foundations of geropsychological assessment: theory and
research informing multiple assessment domains (e.g., mood,
cognition, decision making, and functional capacities)
Foundations of intervention and consultation: theory and
research evidence about geropsychological interventions, aging
services, prevention and health promotion, and models and
methods of interdisciplinary collaboration
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Percent

Serious Psychological Disorders

4.5
4
3.5
3
2.5
2
1.5
1
0.5
0

Total
Men
Women

CDC (2014)
18-44

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45-64

65+

Todays lecture
Differences in psychopathologies of old
adults and younger adults
Age-Related Mental Disorders
Pseudodementia
Delirium
Alzheimers Disease and dementia

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Disorders as observed in older adults

Category
Mood disorders

Description
Disturbance
of mood

Anxiety disorder Intense anxiety

worry, or
apprehension

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Example

Variation in older adults

Major depression
Bipolar disorder
Dysthymia

Generalized anxiety;
disorder; panic
disorder; phobia;
obsessivecompulsive disorder;
post-traumatic stress

Depression may appear as

cognitive complaints or social
isolation; Bipolar disorders
may appear with hostility and
paranoia; most prevalent in
medical settings
Changes in health and
physical symptoms and
interact with symptoms
of anxiety

Disorders as observed in older adults

Category

Description

Schizophrenia
and other
psychotic
disorders

Psychotic
Schizophrenia
symptoms such
Schizoaffective
distortions of
Delusional dis.
reality and serious
impairment in
thinking, behavior,
affect, and motivation

Substancerelated
disorders

Use or abuse of
psychoactive
substances

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Example

Variation in older adults

Shift from positive to negative
symptoms in older adults; depressive
symptoms may coexist with
symptoms of schizophrenia; poorer
cognition than suggested by age

Substance
Older adults at a higher risk than may
dependance;
be thought for these disorders.
substance abuse;
substance intoxication.

Prevalence of various mental

disorders as a function of age
9
8

Prevalence (%)

From Rabins (2002)

18-24 yrs
25-44 yrs
45-64 yrs
65 yrs +

6
5
4
3
2
1
0

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C

Psychopathologies Summary
Prevalence of most disorders significantly less in older
adults.
Mental disorders often have co-mobidities
Depression and anxiety disorders twice as likely in
women as in men
Higher rates of depression associated with older adults in
medical settings
Depression more likely to have accompanying physical
symptoms (insomnia, changes in appetite, diffuse pain,
fatigue, headaches, etc.)
More negative symptoms in schizophrenia (withdrawal,
lack of affect, apathy) than positive (hallucinations and
delusions)
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Late-Onset
Late-onset depression
Mild or moderate depression that starts after age 60.
Risk factors: losing spouse; less than high school education, physical
impairments; heavy alcohol use.
Even though prevalence low in older adults, rise in incidence in 60s.

Late-onset schizophrenia
Not in DSM5 but recognized for adults over 45.
Sometimes call paraphrenia, but very rare
More likely to involve paranoia symptoms, and more likely to respond
to antipsychotic medications.
May be triggered by loss in sensory functioning, making it more likely
for them to misperceive the words and actions of others.

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Pseudodementia

(Depression disguised as Dementia)

DEPRESSIVE
PSEUDODEMENTIA

DEMENTIA

ONSET

Rapid

Progressive, ill-defined

BEHAVIOR

Stable, depression,
apathy, withdrawal

Variable mood, fluctuates

normal and withdrawn

MENTAL COMPETENCE

Highlights amnesia
complaints of memory

Conceals amnesia

SOMATIC SIGNS

Anxiety, insomnia,
eating disorder

Occasional sleep diturb.

PROGNOSIS

Reversible with therapy

Chronic, progressive
decline, not reversible

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Delirium

Disturbance in consciousness (acute state of confusion)

Develops over short period of time
Difficulties with attention, memory, & language
Also affects perception, sleep-wake cycle, personality, &
mood
Can be caused by medical conditions
Can be caused by drugs and anesthesia
Incidence low in community 0.4 - 1.1%, but
high in medical settings (50% of postoperative patients over 65)
https://www.youtube.com/watch?v=hwz9M2jZi_o
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Delirium vs. Dementia

Clinical feature

Delirium

Dementia

Onset

Acute, often at twilight*

Chronic, insidious

Course

Short, diurnal

Long, no diurnal effects

Progression

Abrupt

Slow, but uneven

Duration

Hours to months

Lifetime after onset

Awareness

Reduced

Clear

Attention

Impaired

Normal

Memory

Recent impaired

Recent and remote impaired

Perception

Distorted, delusions

Misperceptions usually absent

Sleep-wake cycle Disturbed, cycle reversed

Fragmented

* Sundowner Syndrome
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Some aging issues about therapy

Older cohorts more skeptical about therapy
process
They are often embarrassed or stigmatized by the
process
Sensory and cognitive loss may impair
communication process
Therapists must be careful not to use elderspeak
Recent research shows that group work is good for
older adults (with peers)
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ALZHEIMERS DISEASE
Charlton Heston & Ronald Reagan

Pat Summitt
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Glen Campbell
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ALZHEIMERS DISEASE
GLEN CAMPBELL
April 8, 2016 Wife says he cannot speak or play
guitar.

At about 11 a.m. ET on Tuesday (April 19, 2016),

our beloved singer Glen Campbell passed away.
YESTERDAY - On Wednesday (April 20) the
singer's reps officially confirmed that
Glen Campbell is not dead.
He joins the long list of celebrities who have
been victimized by this hoax. He's still alive
and well, stop believing what you see on
the Internet, they said.
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Im not going
to miss you
Im here, but yet
Im gone

https://www.youtube.com/watch?v=U8TsAh-zYFI

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ALZHEIMERS DISEASE

PET image of normal

20-year old brain

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PET image of Alzheimers

patients brain

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Alzheimers Disease
Discovered in 1906 by a German neurologist - Alois
Alzheimer
He performed a neurological autopsy of a 56 year old
woman, Auguste Deter. She died after several years
of progressive mental deterioration marked by
increasing confusion and memory loss.
He discovered an odd disorganization of the nerve
cells in her cerebral cortex, the part of the brain
responsible for reasoning and memory.
The cells were bunched up like a rope tied in knots,
which he named "neurofibrillary tangles." He also
noted an unexpected accumulation of cellular debris
around the affected nerves, which he termed
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"senile plaques."

ALZHEIMERS DISEASE (AD)

AD is the only top 10 fatal disease in America that cannot be

prevented, slowed, or cured with current medicine.
AD is a brain disorder which gradually destroys the ability to
reason, remember, imagine, and learn.
In the latter stages of this disease, AD patients no longer
recognize themselves or much about the world around them.
The senile plaques and neurofibrillary tangles take over healthy
brain tissue and devastate the areas of the brain associated with
intellectual functioning.
AD earlier referred to pre-senile dementia, but
now is used to cover senile dementia also (SDAT)
Risk of AD involves

Age
Family history
Genetics
Down Syndrome (Chromosome 21)

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ALZHEIMERS DISEASE
Some media and texts report AD to affect as
many as 50% of those over 85, but
prevalence is less than that.
Zarit and Zarit (1998) report about 2.3 million
cases in US, representing 6.9% of those over
65 and 29% of the oldest old (those over 85).
Other dementias: Vascular dementia, multiinfarct dementia, frontal dementia,
Parkinsons Disease, Picks disease
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ALZHEIMERS DISEASE
Prevalence and racial disparities of Alzheimers Disease

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DHHS (2014)

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Cognitive change by severity of AD:

Memory

Working
Episodic
Remote
Semantic

Language
Visuo-spatial / Perception
Attention / Executive function

Minimal
++
-/+
-/+

Mild
+
+++
-/+
-/+
+
++

Moderate
++
+++
++
+++
+
++
+++

Severe
+++
+++
+++
+++
++
+++
+++

Key: - absent; + present; -/+ variable

From Hodges, J.R. (2000) Memory in the dementias.

In E. Tulving and F.I.M. Craik (Eds.), The Oxford
Handbook of Memory.
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ALZHEIMERS DISEASE

Diagnosis:

Memory Loss
Aphasia language use
Apraxia planned movement
Agnosia process sensory information

Some controversy:
Normal Aging Mild Cognitive Impairment (MCI) AD

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Mini-mental status exam

Folstein et al. (1975)
Indications
1. Cognitive Function Assessment
2. Documentation of subsequent cognitive function decline
Questions (Total of 30 points)
1. Orientation (10 points)
1. Year, Season, Date, Day of week, and Month
2. State, County, Town or City
3. Hospital or clinic, Floor
2. Registration (3 points)
1. Name three obects: Apple, Table, Penny
2. Each one spoken distinctly and with brief pause
3. Patient repeats all three (one point for each)
4. Repeat process until all three objects learned
5. Record number of trials needed to learn all 3 objects
3. Attention and Calculation (5 points)
1. Spell WORLD backwards: DLROW
2. Points given up to first misplaced letter
3. Example: DLORW scored as 2 points only
4. Recall (3 points)
1. Recite the 3 objects memorized in Registration above

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5. Language (9 points)
1. Patient names two objects when they are
displayed
1. Example: Pencil and Watch (1 point each)
2. Repeat a sentence: 'No ifs ands or buts'
3. Follow three stage command
1. Take a paper in your right hand
2. Fold it in half
3. Put it on the floor
4. Read and obey the following
1. Close your eyes
2. Write a sentence
3. Copy the design (picture of 2 overlapped
pentagons)

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Mini-mental status exam

Folstein et al. (1975)
Interpretation of Mini-mental State Score (Maximum: 30)
1. Normal score: 24 or higher
2. Educational and Age Norms
1. Fourth Grade Education
1. Ages 18 to 69: Median MMSE Score 22-25
2. Ages 70 to 79: Median MMSE Score 21-22
3. Age over 79: Median MMSE Score 19-20
2. Eighth Grade Education
1. Ages 18 to 69: Median MMSE Score 26-27
2. Ages 70 to 79: Median MMSE Score 25
3. Age over 79: Median MMSE Score 23-25
3. High School Education
1. Ages 18 to 69: Median MMSE Score 28-29
2. Ages 70 to 79: Median MMSE Score 27
3. Age over 79: Median MMSE Score 25-26
4. College Education
1. Ages 18 to 69: Median MMSE Score 29
2. Ages 70 to 79: Median MMSE Score 28
3. Age over 79: Median MMSE Score 27

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24 - 30
20 - 23
10 - 19
1 - 9
0

normal, depending on age,

education, complaints
mild
moderate
severe
profound

26

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SENILE PLAQUES
Accumulation of amyloid plaques that develop 10
to 20 yrs before cognitive symptoms.
Beta amyloid protein fragments that collect
together in insoluble deposits.
Beta amyloid is formed from a larger protein
found in normal brains called amyloid precursor
protein (APP). It plays an important role in cell
communication and growth.

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NEUROFIBRILLARY TANGLES
Tangles made up of tau protein that
plays role in maintaining microtubules
that form internal support structure of the
axons in nerve cells.
In AD, tau is chemically damaged and
cannot separate and support
microtubules, thus damaging cell
communication and causing neuron
loss.

Earliest tangles seen in hippocampal areas (memory).

Associated loss of neurons can be as high as 90% before
disease runs its full course.

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Just eleven years ago:

PET imaging of amyloid plaques and Tau
Jan. 10, 2004 - UCLA
Amer.J.Ger.Psychiat. (Barrio & Small)
Jan. 22, 2004 - Univ. of Pittsburgh
Annals Neurol.
Pittsburgh Compound B (PIB) (Klunk & Mathis)

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Landau and Jagust (2012)

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Vol. 355

December 21, 2006

No. 25

PET of Brain Amyloid and Tau in

Mild Cognitive Impairment
Gary W. Small, M.D., Vladimir Kepe, Ph.D., Linda M. Ercoli, Ph.D., Prabha Siddarth, Ph.D., Susan Y.
Bookheimer, Ph.D., Karen J. Miller, Ph.D., Helen Lavretsky, M.D., Alison C. Burggren, Ph.D., Greg M. Cole,
Ph.D., Harry V. Vinters, M.D., Paul M. Thompson, Ph.D., S.-C. Huang, Ph.D., N. Satyamurthy, Ph.D., Michael
E. Phelps, Ph.D., and Jorge R. Barrio, Ph.D.

Conclusions FDDNP-PET scanning can differentiate persons with

mild cognitive impairment from those with Alzheimer's disease and
those with no cognitive impairment. This technique is potentially
useful as a noninvasive method to determine regional cerebral patterns
of amyloid plaques and tau neurofibrillary tangles.
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ALZHEIMERS DISEASE
Causes of AD:
Genetics
Environmental

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GENETIC CAUSES OF
ALZHEIMERS DISEASE
Certain families are more prone to developing early onset AD (4055)
Another gene involved in familial AD starting at more conventional
ages (60-65) - apolipoprotein E (ApoE) located on Chromosome
19. It seems to be involved with binding beta amyloid so may play
a role in plaque formation.
People with ApoE 4 allelle of the gene have much higher risk of
AD than those who do not. (largest genetic risk factor)
APP gene on chromosome 21 appears to control production of
protein that produces beta amyloid.
Early onset AD associated with defects in presenilin genes (PS1
[chrom. 14] - 32-56) and (PS2 [chrom. 1] - 40-85). It is believed
that this gene increases beta-amyloid production by APP
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Genetic factors ApoE 4

E2

E4

General
Frequency

8.4%

13.7%

AD Frequency

3.9%

36.7%

Allele (ApoE) on Chromosome 19:

ApoE 2 Protective factor for AD
ApoE 3 most common allele neutral to AD
ApoE 4 Largest genetic risk factor for AD
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ENVIRONMENTAL INFLUENCES
ON ALZHEIMERS DISEASE
Genetic contributions leave unexplained about
60% of late-onset ands 50% of early-onset AD.
Unusual study of 3700 men born between 1900
and 1917 in Japan but lived adult life in Hawaii.
Their prevalence of AD was 5.4%; however, with
men living in Japan, only 1.5%.
High education associated with reduced risk for AD
Nun study - 678 sisters - much lower rate of AD
(highly educated and intellectually active).
One nun (Sister Mary) lilved to 101 and was
cognitively intact even though her brain would have
led to a diagnosis of AD
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Who are the victims of AD?

Patients
Family and friends - Family and friends spend years watching
Alzheimers patients suffer from this progressive, degenerative
disease. A person with Alzheimers lives an average of 8 years
and as many as 20 years or more from the onset of the
symptoms. More than 7 out of 10 people with Alzheimers
disease live at home. Almost 75% of home care is provided by
family and friends.
Employers - Alzheimers disease costs American businesses
more than $33 billion annually--$26 billion is attributed to lost
productivity of caregivers plus $7 billion related to costs for
health and long-term care.
Society - The community loses the knowledge and abilities of the
Alzheimers patients. In addition, the United States spends at
least $100 billion a year on the disease. Neither Medicare nor
private health insurance covers the type of long-term care most
patients need.

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Drug treatments for AD

Between 1998 and 2014, 101
unsuccessful attempts to develop drugs
to treat Alzheimers Disease
During that time, only 23 drugs
approved to treat symptoms
Most approved drugs slow progression
of AD very slightly in a few people
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Drug treatment
Although there is no cure, Alzheimer's medications (cholinesterase
inhibitors) can temporarily slow the worsening of symptoms and improve
quality of life in some patients with Alzheimer's and the quality of life in their

caregivers.
Drug name

Brand name

Approved For

1. donepezil

Aricept

All stages

2. galantamine

Razadyne

Mild to moderate

FDA Approved
1996
2001

3. memantine

Namenda

Moderate to severe
2003

4. rivastigmine

Exelon

All stages
2000

5. donepezil and
memantine

Namzaric

Moderate to severe

There is no evidence that NAMZARIC (#5) prevents or slows the

underlying disease process in patients with Alzheimer's disease.
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2014

38

Much research,
with many new, recent findings
4/2016 - Study has discovered that a protein called IL-33
can reverse Alzheimer's disease like pathology and
cognitive decline in mice.
3/2016 - Researchers show how brain connections, or
synapses, are lost early in Alzheimer's disease and
demonstrate that the process starts -- and could potentially
be halted -- before telltale plaques accumulate in the brain.
10/2015 - A new study has identified a number of genes
that are repressed at various time points after memory
formation, providing important clues as to how long-term
memories are formed.
This year (2/2016) special issue of TIME magazine
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39

Feb./ 2016
Frank Longo (Stanford)
New drug (LM11A-31)
featured by TIME
Doesnt attack plaque,
but keeps brain cells
healthy (nerve growth
factors).
Now in Phase II
clinical trials
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Memory Intervention
Spaced retrieval (SR)

Cameron Camp
Center for Applied Research
in Dementia
Solon, Ohio (Cleveland)

Show picture of person and say name

5 sec. later, show picture and ask for name
If person remembers, recall interval increased
If person fails to remember, recall interval decreased
During recall intervals, the instructor engages patient with
conversation
Spaced retrieval works well; AD patients can be taught all
kinds of information
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In Summary, we have discussed:

Differences in Mental Disorders for
Different Age Groups
Prevalence of Mental Disorders by Age
Pseudodementia, Delirium, and Dementia
Alzheimers Disease (AD)
Diagnosis, Causes, and Treatment of AD
A Memory Intervention for AD: Spaced
Retrieval
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Questions?

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