Details of Alzheimer's Disease and Etiology of Protein. Under the guidance of Mr. Nilanjan Adhikari Assistant professor,Department of Pharmacology P.G INSTITUTE OF MEDICAL SCIENCES

1. Etiology of TAU and
PLAQUE protein in
Alzheimer’s
Ansar Laskar
B.pharm, Final Year
Under the Guidance of
Mr. Nilanjan Adhikari
Assistant Professor
Department of Pharmacology of P.G. Institute of Medical Sciences
Presented by

2. 1. Alzheimer’s Disease
 Introduction
 Changes in Brain
 Causes of AD
 Diagnosis & Treatment of AD
2. Aim
3. Objective
 Clinical Hallmark of AD
Beta amyloid Plaque
Neurofibrillary Tangles
4. Conclusion
5. Reference
Contents:

3. Introduction:
Alzheimer’s Disease:
 Alzheimer’s Disease is a progressive neurodegenerative disease
discovered by Alois Alzheimer, in 1906.
Brain cell are progressively damaged leading to loss of memory,
thinking skills, etc.
Disease was identified more than 100 years ago, which associated with
dementia like symptoms.
 Dementia ????
So in this disease a person might forget where he kept his car keys, the
way of his home, impaired reasoning of judgement, difficulty in facial
recognition.

4. Changes in Brain:
Gyri become narrower.
Sulci get widened.
Ventricles get severely enlarged.
Figure 1: Progression of Alzheimer’s Disease[8]

5. Causes of AD:
Alzheimer’s disease is caused by a combinational of genetic
lifestyle and environmental factors that affect the brain over time.
At a fundamental level, brain protein fail to function normally.
Which disrupts the work of brain cells(neurons) and trigger a series
of harmful events.
Causes of Alzheimer’s disease are focused on the role of two
protein that is:
 β-amyloid protein- Beta-amyloid is a fragment of a larger protein.
When these fragments cluster together, they appear to have a toxic
effect on neurons and to disrupt cell-to-cell communication.
 TAU Protein- Tau proteins play a part in a neuron's internal support
and transport system to carry nutrients and other essential
materials.
Another causes is dysfunctional cholinergic neurons and they
release less acetylcholine in the synaptic cleft and because of these
there reduce cholinergic transmission, due to reduce cholinergic
transmission neuronal death occurs.

6. Doctors will look at the signs and symptoms take a medical history and rule out
other conditions before making a diagnosis.
Check the person’s neurological function for example by testing their balance,
senses and reflexes other assessments may includes a blood and urine test.
Perform brain scans such as : CT, MRI, PET etc.
Diagnosis of AD
Treatment of AD
Currently there is no cure for Alzheimer’s. Treatments aim to slow down the
process of destruction and relieve symptoms to improve quality of life for
patients.
Alzheimer’s medications can help for a time with memory symptoms and other
cognitive changes .
Two types of drugs are currently used to treat cognitive symptoms
 Cholinesterase inhibitors.
 Memantine(Namenda).
 Clozapine, Haloperidol are used to treat non-cognitive Symptoms.

7. Aim:
Objective:
Clinical hallmarks of Alzheimer’s Disease:
 clinical hallmarks involve Beta amyloid plaques and neurofibrillary
tangles.
 Beta amyloid plaque:
 Amyloid precursor protein(APP) is a part of nerve cell membrane which
required for nerve growth and repaired, this APP is broken into fragments and
these fragments removed from the body by two pathways-
 Non-amyloidogenic pathway : Responsible enzymes are α-secretase
and γ-secretase.
 Amyloidogenic pathway : the two enzymes named β-secretase and γ-
secretase.
 In amyloidogenic pathway β-secretase enzymes breaks APP in such a way that
a comparatively larger fragment, which is called as beta amyloid protein.
In questing the hypothesis on clinical establishment in the etiology of
plaque and TAU proteins in Alzheimer’s.

8. This β-amyloid protein is made up of 36 to 43 amino acid, due to larger in size
this protein is also very sticky.
In Alzheimer’s Disease:
Excessive formation of β-amyloid protein
Reduced removal of β-amyloid protein
Accumulation of these protein in the neuronal junction
Form plaques which resulting in progressive neurodegeneration.
Neurofibrillary Tangles:
The function of microtubules is the intracellular transportation.
Tau protein is responsible for the stabilization of microtubules in nerve cells.
In Alzheimer’s there is excessive formation of beta amyloid protein, now this
protein activate intracellular kinase which causes phosphorylation of tau
protein.
After phosphorylation it detached itself from microtubules.
They aggregates together to form neurofibrillary tangles because of the
formation of tangles there is de-stabilization of microtubules.
Which disrupts the normal intracellular transport mechanism.

9. Figure 2: Location of PLAQUE and TANGLE[9]

10. Alzheimer’s disease is the most common form of dementia in older adults. The
etiology of the disease is too much fishy yet. The procurements of AD with
drug developments need further assessment to layout the hypothetically
establishment of the disorder.
Remarkable progress is going on, but needs to more exploration for
questing advanced treatment sustaining many more miles to go.
Conclusion:

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8. Figure 1: https://www.thehelperbees.com/individuals/healthy-hive/alzheimers-and-the-importance-of-
brain-health/ Date: 15.05.2022 Time: 11:25 am.
9. Figure 3: https://www.molecularcloud.org/p/il3-in-astrocyte-and-microglia-communication-a-potential-
therapeutic-target Date:20.05.2022Time:07:00pm.
Reference:

12. Thank you