2. Alzheimer’s disease is an irreversible,
progressive brain disease that slowly
destroys memory, thinking skills and
eventually even the ability to carry out
the simplest tasks in routine.
It is one of the major neurodegenerative
disorders in the present era.
3. First person to report AD was a
German psychiatrist Alois Alzheimer.
Most common cause of dementia
among people above 65 yrs of age.
In 2015, there were approximately 48
million people worldwide with AD
4. Etiology – exact cause still unknown
Risk factors
▪ Age
▪ Genetics
▪ Lifestyle
5. 1. Early onset AD
▪ Rare
▪ Usually affecting people aged 30 to 60
▪ Usually running in families
2. Late onset AD
▪ Common
▪ Usually affects people over 65 yrs of age
6. • The brain has billions of
neurons, each with an axon
and many dendrites.
• To stay healthy, neurons
must communicate with
each other
7. The brains of people with AD have an
abundance of two abnormal structures:
1. Beta-amyloid plaques - dense deposits
of protein and cellular material that
accumulate outside and around nerve
cells
2. Neuro fibrillary tangles - twisted fibers
that build up inside the nerve cell
8. Beta-amyloid Plaques
Amyloid precursor protein (APP) is the
precursor to amyloid plaque.
1. APP sticks through the neuron
membrane.
2. Enzymes cut the APP into fragments
of protein, including beta-amyloid.
3. Beta-amyloid fragments come together
in clumps to form plaques.
In AD, many of these clumps form,
disrupting the work of neurons. This affects
the hippocampus and other areas of the
cerebral cortex.
9. Neurons have an internal support structure partly made up of
microtubules. A protein called tau helps stabilize microtubules. In
AD, tau changes, causing microtubules to collapse, and tau proteins
clump together to form neurofibrillary tangles.
10.
11.
12.
13. 1. Prodormal symptoms/ Pre dementia
2. Early stage/ MildAlzheimer's
3. Middle stage/ ModerateAlzheimer's
4. Late stage/ SevereAlzheimer's
14. Not remembering episodes of forgetfulness
Forgets names of family or friends
Changes may only be noticed by close friends or
relatives
Some confusion in situations outside the familiar
15. Greater difficulty remembering recently
learned information
Deepening confusion in many circumstances
Problems with sleep
Trouble knowing where they are
16. Poor ability to think
Problems in speaking
Repeats same conversations
More abusive, anxious, or paranoid
17. Detailed history and examination
Eight cognitive domains
▪ Memory
▪ Language
▪ Perceptual skills
▪ Attention
▪ Constructive abilities
▪ Orientation
▪ Problems solving
▪ Functional abilities
Neuropsychological tests – Mini mental state
examination
Investigations – MRI, PET scan
18.
19. No direct reference for AD
On the basis of its clinical presentation, it
can be correlated with different entities
SingleAyurvedic corelation- Difficult
27. Ritu shodhana for prevention and to arrest
progression
Snehapana – Kalyanaka gritha (AH U 6/26)
Mahakalyanaka gritha (A H U 6/28)
Brahmi gritha (A H U 6/23)
Panchagavya gritha (A H U 7/18)
Mahapaishachika gritham
Purana gritha
28. Vamana and virechana – age to be
considered (7yrs to 70yrs)
Nasya - Brahmi gritha
- Jyothishmati thaila
- Anu thailam
- Shadbindu thailam
Basti – Yapana basti - Mustadi yapana basti
- Raja yapana basti….
Ksheera basti (guduchi )
Matra basti - for prevention
Any score greater than or equal to 24 points (out of 30) indicates a normal cognition. Below this, scores can indicate severe (≤9 points), moderate (10–18 points) or mild (19–23 points) cognitive impairment.[21]