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Am I having dementia? Can I
prevent it?
Current understanding of
Alzheimer’s disease
DR. RUCHIR DIVATIA, M.D.,D.M. – NEUROLOGY (SCTIMST, TRIVANDRUM)
DEPARTMENT OF NEUROLOGY, K.D. HOSPITAL
We are who we are because of
what we learn and what we
remember
Eric Kandel (Famous neurobiologist)
Global burden of neurological disease
Neurological diseases – DALYs by age
Higher cognitive functions
Frontal lobe –
Executive function
Attention
Temporal lobe –
Language, Memory
Parietal lobe – Praxis,
Language
Occipital lobe –
Visuospatial orientation
How to recognise problems with higher
cognitive functions?
Cognitive domain Problems encountered
Executive Mislead by false advertisements, difficulty planning outing, function, maintaining
bank balance
Attention Forgetting everyday actions, difficulty concentrating, following plot of movie,
maintaining train of thought, recalling why they entered a room
Memory Forgets recent conversations/events, making repetitive statements, using lists,
misplace objects
Language Reduced vocabulary, word finding difficulty, using incorrect words, difficulty
following instructions
Praxis Difficulty with manual skills, clumsiness, inability to dress
Visuospatial Difficulty finding places, objects directly in front, inability to recognise familiar faces,
bumping into walls, poor driving
What are the types of memory?
A. Declarative/Explicit (Consciously evoked)
1. Episodic (Ability to store & retrieve past episode & experiences)
2. Semantic (General knowledge of people, objects, words, concepts)
B. Non declarative/Implicit (memories that do not need conscious
involvement)
1. Procedural memory – motor skills
C. Working memory – Ability to keep information trace active on the
brain for short period (executive function)
How is memory stored?
How to test for
cognitive function?
How much cognitive decline is “normal” with
aging?
What is mild cognitive impairment?
• Transition state between normal cognition in older adult and
dementia
1. Is the cognitive symptom clearly a decline from patient’s previous
cognitive level?
2. Is the cognitive symptoms consistent?
3. Does the symptom have a clear effect on the patient’s day-to-day
function?
4. Does the patient show clear evidence of impairment on cognitive
assessment?
NORMAL COGNITION ↔ MILD COGNITIVE IMPAIRMENT → DEMENTIA
When to diagnose Dementia?
When to suspect a reversible cause of dementia?
• DEPRESSION SHOULD ALWAYS BE EXCLUDED FIRST
• Rapid unexplained decline
• Younger than expected age at symptom onset
• Prominent fluctuations
• High risk exposures (Drugs, alcohol)
• High risk behaviours
• Unexplained/Unanticipated findings on examination
• Incongruent cognitive testing
What happens in the brain in AD?
Amyloid beta PET scan in AD
Biomarkers for diagnosis of AD
Symptoms progression in AD
Alzheimer’s Disease – risk factors &
associations
Non
modifiable
Modifiable Emerging Bidirectional Associations
Age Hypertension Air pollution Hearing impairment
Female
gender
Diabetes Mellitus, Obesity,
smoking, Alcohol
Traumatic brain injury Insomnia, Sleep disturbances,
short sleep
Ethnicity Diet Late life depression Epilepsy
APOE gene Limited cognitive, physical &
social activities
Delirium
APP, PSEN1,
PSEN2 gene
low education
Hearing impairment ↔ Dementia
• Hearing – complex cognitive function
• Pre cognitive processing → Auditory objects → Auditory cognition
• Extensive efferent regulation of afferent pathways
• Non linear relations of auditory signals
• ‘Speech in noise’ perception a preclinical marker
Pathophysiology of hearing impairment &
dementia
Sleep disorders ↔ Alzheimer’s Disease
• Advanced AD → Changes in suprachiasmatic nucleus→ Irregular sleep
wake cycle
• Shorter (≤5 hours) & Longer(≥10 hours) sleep duration → Increased
inflammatory markers (CRP, IL-6)→ Impaired cognitive function
• ↑Aβ deposition, ↓ Aβ Clearence (improved by lateral decubitus in
mice model)
• ↑ Biomarkers of cellular ageing (contributes to biological ageing)
Temporal lobe epilepsy ↔ Mild Cognitive
Impairment
• Late onset TLE (LO-TLE) had similar pattern and magnitude of atrophy
as MCI
• LO-TLE & MCI – significant memory & language impairment
• LO-TLE – More consistent cortical thinning than Early onset TLE
• Histopathology in TLE – Aβ precursor protein & tau
• Aβ tied to epileptiform activity
• Silent seizures in subset of patients with AD
Leisure activity & risk of Dementia
Type of leisure activity Example Role in dementia prevention
Stimulating activity Doing crosswords, Playing cards,
Attending organizations, Practising
artistic activities
50% reduction in risk
Social support activity Visiting/inviting friends, relatives ↓ in low education, vascular
cognitive impairment
Physical leisure activity Doing odd jobs, Gardening, Walk
Passive leisure activity Watching TV/Mobile, listening to
radio/music, Knitting/sewing
Don’t contribute to Cognitive
reserve as stimulating activities
Association of each leisure activity in 1997–1999 with subsequent incident dementia
Andrew Sommerlad et al. Neurology 2020;95:e2803-e2815
Copyright © 2020 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the
Diet and Dementia – Diet inflammatory index
Pro vs Antiinflammatory foods
Proinflammatory foods Antiinflammatory foods
Meat Fiber (Fruits, vegetables, beans, nuts, seeds)
Refined carbohydrates (White breads, white rice,
sweetened beverages, colas)
Phytonutrients (Red, orange, yellow vegetables &
fruits, turmeric, curcumin, pepper, garlic, ginger,
onion, green tea, black coffee)
Healthy fats (Olive oil, sesame oil, omega-3-fatty acids,
Walnuts, Flaxseeds)
Summary of protective vs risky factors for AD
Understaing memory  alziemer diseasepptx

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Understaing memory alziemer diseasepptx

  • 1. Am I having dementia? Can I prevent it? Current understanding of Alzheimer’s disease DR. RUCHIR DIVATIA, M.D.,D.M. – NEUROLOGY (SCTIMST, TRIVANDRUM) DEPARTMENT OF NEUROLOGY, K.D. HOSPITAL
  • 2. We are who we are because of what we learn and what we remember Eric Kandel (Famous neurobiologist)
  • 3. Global burden of neurological disease
  • 5. Higher cognitive functions Frontal lobe – Executive function Attention Temporal lobe – Language, Memory Parietal lobe – Praxis, Language Occipital lobe – Visuospatial orientation
  • 6. How to recognise problems with higher cognitive functions? Cognitive domain Problems encountered Executive Mislead by false advertisements, difficulty planning outing, function, maintaining bank balance Attention Forgetting everyday actions, difficulty concentrating, following plot of movie, maintaining train of thought, recalling why they entered a room Memory Forgets recent conversations/events, making repetitive statements, using lists, misplace objects Language Reduced vocabulary, word finding difficulty, using incorrect words, difficulty following instructions Praxis Difficulty with manual skills, clumsiness, inability to dress Visuospatial Difficulty finding places, objects directly in front, inability to recognise familiar faces, bumping into walls, poor driving
  • 7. What are the types of memory? A. Declarative/Explicit (Consciously evoked) 1. Episodic (Ability to store & retrieve past episode & experiences) 2. Semantic (General knowledge of people, objects, words, concepts) B. Non declarative/Implicit (memories that do not need conscious involvement) 1. Procedural memory – motor skills C. Working memory – Ability to keep information trace active on the brain for short period (executive function)
  • 8. How is memory stored?
  • 9. How to test for cognitive function?
  • 10. How much cognitive decline is “normal” with aging?
  • 11. What is mild cognitive impairment? • Transition state between normal cognition in older adult and dementia 1. Is the cognitive symptom clearly a decline from patient’s previous cognitive level? 2. Is the cognitive symptoms consistent? 3. Does the symptom have a clear effect on the patient’s day-to-day function? 4. Does the patient show clear evidence of impairment on cognitive assessment? NORMAL COGNITION ↔ MILD COGNITIVE IMPAIRMENT → DEMENTIA
  • 12. When to diagnose Dementia?
  • 13. When to suspect a reversible cause of dementia? • DEPRESSION SHOULD ALWAYS BE EXCLUDED FIRST • Rapid unexplained decline • Younger than expected age at symptom onset • Prominent fluctuations • High risk exposures (Drugs, alcohol) • High risk behaviours • Unexplained/Unanticipated findings on examination • Incongruent cognitive testing
  • 14. What happens in the brain in AD?
  • 15.
  • 16. Amyloid beta PET scan in AD
  • 19. Alzheimer’s Disease – risk factors & associations Non modifiable Modifiable Emerging Bidirectional Associations Age Hypertension Air pollution Hearing impairment Female gender Diabetes Mellitus, Obesity, smoking, Alcohol Traumatic brain injury Insomnia, Sleep disturbances, short sleep Ethnicity Diet Late life depression Epilepsy APOE gene Limited cognitive, physical & social activities Delirium APP, PSEN1, PSEN2 gene low education
  • 20. Hearing impairment ↔ Dementia • Hearing – complex cognitive function • Pre cognitive processing → Auditory objects → Auditory cognition • Extensive efferent regulation of afferent pathways • Non linear relations of auditory signals • ‘Speech in noise’ perception a preclinical marker
  • 21. Pathophysiology of hearing impairment & dementia
  • 22. Sleep disorders ↔ Alzheimer’s Disease • Advanced AD → Changes in suprachiasmatic nucleus→ Irregular sleep wake cycle • Shorter (≤5 hours) & Longer(≥10 hours) sleep duration → Increased inflammatory markers (CRP, IL-6)→ Impaired cognitive function • ↑Aβ deposition, ↓ Aβ Clearence (improved by lateral decubitus in mice model) • ↑ Biomarkers of cellular ageing (contributes to biological ageing)
  • 23.
  • 24. Temporal lobe epilepsy ↔ Mild Cognitive Impairment • Late onset TLE (LO-TLE) had similar pattern and magnitude of atrophy as MCI • LO-TLE & MCI – significant memory & language impairment • LO-TLE – More consistent cortical thinning than Early onset TLE • Histopathology in TLE – Aβ precursor protein & tau • Aβ tied to epileptiform activity • Silent seizures in subset of patients with AD
  • 25. Leisure activity & risk of Dementia Type of leisure activity Example Role in dementia prevention Stimulating activity Doing crosswords, Playing cards, Attending organizations, Practising artistic activities 50% reduction in risk Social support activity Visiting/inviting friends, relatives ↓ in low education, vascular cognitive impairment Physical leisure activity Doing odd jobs, Gardening, Walk Passive leisure activity Watching TV/Mobile, listening to radio/music, Knitting/sewing Don’t contribute to Cognitive reserve as stimulating activities
  • 26. Association of each leisure activity in 1997–1999 with subsequent incident dementia Andrew Sommerlad et al. Neurology 2020;95:e2803-e2815 Copyright © 2020 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the
  • 27. Diet and Dementia – Diet inflammatory index
  • 28. Pro vs Antiinflammatory foods Proinflammatory foods Antiinflammatory foods Meat Fiber (Fruits, vegetables, beans, nuts, seeds) Refined carbohydrates (White breads, white rice, sweetened beverages, colas) Phytonutrients (Red, orange, yellow vegetables & fruits, turmeric, curcumin, pepper, garlic, ginger, onion, green tea, black coffee) Healthy fats (Olive oil, sesame oil, omega-3-fatty acids, Walnuts, Flaxseeds)
  • 29. Summary of protective vs risky factors for AD

Editor's Notes

  1. Association of each leisure activity in 1997–1999 with subsequent incident dementia CI = confidence interval; HES = hospital episode statistics; HR = hazard ratio.