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Understanding the Person with Dementia
Oxford Brookes University
What is dementia?
How do we diagnose it?
What can we do?
Sharon Christie
OPTIMA, University of Oxford
Oxford Memory Assessment Clinic
DEMENTIA – AN EPIDEMIC
•Estimated that at least 15 million people are
affected worldwide
•In the UK there are about 800,000 people
with dementia, nearly 2/3 of whom have AD
•Age is biggest risk factor:
1 in 6 in people over 80yrs old
1 in 25 from 70-79yrs old
1 in 100 from 60-69yrs old
•But some people are affected at a much
earlier age (1 in 1400 between 40 – 64yrs
old)
WHAT IS DEMENTIA?
•Dementia describes a set of symptoms
•Dementia is a syndrome rather than a
diagnosis
•Dementia is not part of normal ageing
•It is caused by diseases of the brain
The cause gives us a diagnosis usually
probable or possible
What is Dementia?
‘an acquired, global impairment of
intellect, memory and personality
without impairment of consciousness’
Impacts on normal social and/or
occupational functioning
Impairment is sustained over time
(progressive)
EARLY CHANGES
•Not remembering appointments
•Misplacing items
•Difficulty remembering recent information or
events
•Not recognising faces
•Word-finding difficulty
•Lack of concentration
•Difficulty making decisions
•Losing track of time
•Mistakes in judgement
CHANGES
•Withdrawal / lack of confidence
•Apathy / lacking motivation
•Irritability / frustration
•Lose thread of conversation or rambling sentences
•Accusatory or paranoid
•Unable to sequence tasks
•Difficulty reading or writing
•Reacting less quickly
•Supervision with Activities of Daily Living (ADL)
WHY ARE PEOPLE NOT REFERRED FOR
ASSESSMENT?
•41% of people with dementia do not
have a diagnosis
•Dementia still has a stigma for some
people and in society generally
•Anxiety and fear of getting a diagnosis
•Lack of insight and denial of a problem
•Some people assume nothing can be
done so may not seek help
•GPs may not refer
SPECIALIST ASSESSMENT
GP may refer to:
•Neurology
•Geratology
•Old Age Psychiatry / Community Mental Health Team
Memory Clinics:
•History including collaborative
•Mental state examination
•Cognitive testing
•Physical examination inc. neurological exam
•Blood screen
•Scans/Imaging : CT / MRI / PET / DAT
NORMAL AGEING
•From adulthood, memory shows a slow
progressive impairment
•Processing is slower
•? Reduced ability to learn new things
MILD COGNITIVE IMPAIRMENT
MCI – between normal ageing & dementia
Petersen criteria (2001):
Subjective memory complaint – corroborated by
informant
Objective memory impairment for age
(1.5 below standard deviation for normal ageing)
Does NOT interfere with Activities of Daily Living
NEED TO RULE OUT / CONSIDER:
•Brain Tumour
•Brain Haemorrhage
•Normal Pressure Hydrocephalus
•Alcohol abuse
•Drug interactions
•Infection
•Metabolic disorders
•Endocrine imbalance(eg low thyroxine)
•Poor nutrition / dehydration (eg low Vit. B12)
•Trauma
•Depression
•Anxiety / stress
DEMENTIA
•Cognitive Impairment
•Progressive
•No other cause found
•Affecting function
Dementia: major causes estimated from
clinical diagnoses
Alzheimer’s disease
(62%)
Vascular dementia
(17%)
Mixed dementia (AD & Vascular)
(10%)
Lewy body dementia
(4%)
Other rarer forms
(5%)
eg Fronto-temporal dementia, Korsakoffs, CJD
Alzheimer’s first patient
Alzheimer first saw August D. in
November 1901: she displayed
memory loss and delusions.
She died in 1906.
Alzheimer described the unique
histopathology in 1907: the brain
contained both plaques
(amyloid) and neurofibrillary
tangles (abnormal tau protein).
ALZHEIMER-TYPE PATHOLOGY
Silver stained
plaques and
tangles
•Thick arrow:
senile (neuritic)
plaque
•Small arrow:
diffuse plaque
•Star: tangle
ADAD - PATTERN OF DEGENERATION PATTERN OF DEGENERATION
Accuracy versus p.m. diagnosis 80%
Rapid atrophy of medial temporal lobe in AD
At presentation
later
MMSE 23
7 years
Structural MRI
structural MRI shows the “shape” of
the brain…
Healthy elderly
mild AD
moderate AD
64
67
62
Fronto-temporal dementia
Cerebro-Vascular Damage
Small vessel disease
Lewy Body
DEMENTIA WITH LEWY BODIES
(DLB)
•Build-up of Lewy bodies – accumulated bits of
alpha-synuclein protein - inside the nuclei of
neurons in areas of the brain that control
particular aspects of memory and motor
control.
•Alpha-synuclein accumulation is also linked to
Parkinson's disease
•Similarity of symptoms between DLB and
Parkinson’s disease, and between DLB and
Alzheimer’s disease, can often make it difficult
to make a definitive diagnosis.
DEMENTIA WITH LEWY BODIES (DLB)
•Central feature is progressive cognitive
decline
•Combined with three additional defining
features:
•fluctuations in alertness and attention
•recurrent visual hallucinations
•parkinsonian motor symptoms eg rigidity
and the loss of spontaneous movement.
DIFFERENTIAL DIAGNOSIS
AD: gradual onset / decline
Episodic memory, poor orientation,
Vascular: sudden, stepwise deterioration;
area affected; attention, speed, praxis,
visual-spatial,
FTD: personality & behaviour
IMPORTANCE OF EARLY ASSESSMENT & DIAGNOSIS
•Seek reversible causes
•Identify exacerbating or contributory factors e.g.
•vitamin deficiencies or hormonal problems
•Some types of heart or blood vessel disease
•Options for drug treatments
•To allow patients and families to plan, e.g. financial
and legal issues, future care preferences
•Advice about coping strategies
•Access to support from NHS, Social & Healthcare
Services, Voluntary bodies (e.g. AS, Age UK, Young
Dementia UK), & others
WHAT CAN WE DO MEDICALLY?
•Treat vascular risk factors:
•Control BP
•Control diabetes
•Treat heart conditions
•Stroke prevention eg aspirin
•Correct vitamin deficiencies
WHAT CAN WE DO MEDICALLY?
Treatments for Alzheimer’s disease:
Cholinesterase Inhibitors (ChEI):
•Improve chemical messenger levels in brain
•Donepezil
(Aricept)
•Galantamine
(Reminyl)
•Rivastigmine
(Exelon)
•for mild to moderate AD
•50% +/- response rate; 18-24 months
ChEI treat symptoms, not the disease
WHAT CAN WE DO MEDICALLY?
Treatments for Alzheimer’s disease:
Memantine (Ebixa) - NMDA receptor antagonist
•It blocks the chemical glutamate, which is released in excessive
amounts when brain cells are damaged in AD, and causes further
damage to the cells.
•For moderate to severe AD
Can also be added to ChEI but not currently
available on NHS unless for behavioural symptoms
WHAT ELSE CAN WE DO?
Provide information, support and advice
nurse)
Clinical staff at clinic
(Doctors, memory clinic
Dementia Advisor at clinic (O.C.C/ Alz Soc/ Age UK)
Information about the disease & symptoms
Coping strategies for person with dementia and family
Driving
Power of Attorney / legal matters / finances, benefits
Dementia Information Line
Carer support group information
Services, activities,
WHAT CAN WE DO?
•Research into new drugs to protect brain cells, rather
than just improve symptoms by helping cells to cope with
damaged chemical messenger systems
•Can we interfere / stop the development of amyloid
plaques and neurofibrillary tangles (abnormal tau protein)?
•Try to identify people with Alzheimer’s disease processes
in their brain before they develop dementia
Jack et al, Lancet Neurology, Jan 2010
Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological
cascade
OXFORD PROJECT TO INVESTIGATE MEMORY &
AGEING
A LONGITUDINAL OBSERVATIONAL COHORT FOUNDED
PROTOCOL / DATA GATHERED
1988
Annual Assessments including:
•Full physical examination
•Scans - CT , MRI, SPECT
•Blood tests (clinical & research)
•Blood pressure measurement
•Height Weight
•Urinalysis
•Cognitive tests
•Questionnaires with study partner
•Lumbar puncture
•Additional 6 monthly cognitive testing and questionnaires
for participants with memory problems
OPTIMA 2009 – A NEW CHAPTER
Completion/continuation of analysis of
longitudinal data
Rationalising of existing longitudinal cohort &
recruitment (including from VITACOG study)
to create a ‘New Cohort’
Longitudinal Early AD cohort
(LEAD cohort)
LEAD 2012 – THE NEXT CHAPTER
•Continue LEAD cohort
•Run alongside OXVASC
•Comparative groups
•Recognition that vascular risk factors
contribute to Alzheimer’s Disease
•Working towards community based
cohort of people with cognitive problems
ONGOING RESEARCH JOURNEY
•LEAD
protocol
participants continue annual assessments as per
•We gather observational and longitudinal data
•Participant has opportunities to participate in new or add-on
studies
•Opportunities to participate in clinical trials of new drugs
•Opportunity to join Brains for Dementia Research
(to donate brain at time of death for research)
POST-MORTEM BRAIN DONATION
•Consider PM consent at each contact
•Ongoing contact enhances possibility of PM consent
•Information of what to do at time of death left with
families, GP & nursing home
•At time of death – always a nurse from OPTIMA
available to facilitate PM procedure
•When neuropathology report available:
Feedback of results to family (face to face,
telephone or written) by nurses
Brains For Dementia Research (BDR)
Oxford is one of 6 centres
How to look after your
memory and reduce your risks of
developing dementia
What is good for your heart is good for your brain!
• Keep mentally active – do crosswords, sudoku, quizzes
• Keep physically active – at least 30 mins of exercise 3 times per week, it
is never too late to start!
• Teenagers: get active now! Activity and exercise during your teenage
years will help keep your memory healthy when you are older.
• Eat a Mediterranean diet with lots of fruit and vegetables, olive oil
• Remain a healthy weight, or lose weight if needed
• Keep happy