Understanding the Person with Dementia Oxford Brookes University

1. Understanding the Person with DementiaOxford Brookes University What is dementia? How do we diagnose it? What can we do? Sharon Christie OPTIMA, University of Oxford Oxford Memory Assessment Clinic

2. 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) DEMENTIA – An Epidemic

3. 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?

4. 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)

5. 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 Early Changes

6. 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) Changes

7. 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 Why are people not referred for assessment?

8. 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 Specialist Assessment

9. From adulthood, memory shows a slow progressive impairment Processing is slower ? Reduced ability to learn new things Normal Ageing

10. 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 Mild Cognitive Impairment

11. 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 Need To Rule Out / Consider:

12. Cognitive Impairment Progressive No other cause found Affecting function Dementia

13. 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

14. 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).

15. Silver stained plaques and tangles • Thick arrow: senile (neuritic) plaque • Small arrow: diffuse plaque • Star: tangle Alzheimer-type pathology

16. ADAD - Pattern of degeneration - Pattern of degeneration

17. Accuracy versus p.m. diagnosis 80%

18. Rapid atrophy of medial temporal lobe in AD At presentation 7 years later MMSE 23 MMSE 13

19. Structural MRI structural MRI shows the “shape” of the brain… Healthy elderly 64 mild AD 67 moderate AD 62

20. Fronto-temporal dementia

21. Cerebro-Vascular Damage

22. Small vessel disease

23. Lewy Body

24. 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)

25. 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.  Dementia with Lewy Bodies (DLB)

26. AD: gradual onset / decline Episodic memory, poor orientation, Vascular: sudden, stepwise deterioration; area affected; attention, speed, praxis, visual-spatial, FTD: personality & behaviour Differential Diagnosis

27. 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 Importance of early assessment & Diagnosis

28. Treat vascular risk factors: Control BP Control diabetes Treat heart conditions Stroke prevention eg aspirin Correct vitamin deficiencies What can we do medically?

29. 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?

30. 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 can we do medically?

31. Provide information, support and advice Clinical staff at clinic (Doctors, memory clinic nurse) 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 else can we do?

32. 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 What can we do?

33. Jack et al, Lancet Neurology, Jan 2010 Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade

34. PROTOCOL / DATA GATHERED 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 Oxford Project To Investigate Memory & AgeingA longitudinal observational cohort founded 1988

35. 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) OPTIMA 2009 – A New Chapter

36. 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 LEAD 2012 – The Next Chapter

37. LEAD participants continue annual assessments as per protocol 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) Ongoing Research Journey

38. 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 Post-mortem Brain Donation

39. 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 Sleep well – address any sleep problems Stay socially connected with friends and family Give up smoking