Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. It is the most common cause of dementia among older adults. The main risk factor is age, with most cases occurring in people over 65 years of age. Pathologically, it is characterized by amyloid plaques and neurofibrillary tangles in the brain that lead to the loss of connections between neurons and ultimately the death of neurons. Currently, there is no cure for Alzheimer's, and available treatments can only temporarily slow the worsening of dementia symptoms. Researchers are studying new therapies targeting the underlying causes and progression of the disease.

1. By:-Deepansha
M.Pharma 2nd semester

2. Alzheimer’s
 The deterioration of intellectual capabilities, memory,
judgment, and personality to the extent that daily
functioning and quality of life are seriously impaired.
 Generally occurs in the elderly impairing brain function,
which can lead to dementia.
 Named for German neurologist Alois Alzheimer in 1907.

3. Statistics
 4 million or more cases in U.S.
 100,000 die each year.
 4th major leading cause of death
in U.S.
 65 or older when symptoms can
begin

4. Clinical Features
 Loss of short-term memory and ability to create memories
 Concentration on past
 Loss of time
 Communication diminishes
 Personality changes
 Delusions
 Become immobilized and uncomprehending
 Death due to respiratory failure
 65 and up disease lasts 8-20 years
 65 and down disease lasts 5-10 years disease more rapid

5. Histological Analysis
3 distinctive neuropathological features
1. Devastating losses of synapses and neurons within
hippocampus and entorhinal cortex.
2. Dense spherical structures, called senile plaques (SP),
prevalent outside the neurons of the hippocampus and
other regions of the brain.
3. Aggregations of fibrils (Neurofibrillary tangles, NFT)
accumulate within cell bodies and dendritic processes of
the neurons of the hippocampus, neurocortex,
entorhinal cortex, and other brain parts.

6. Neuropathology-

7. Pictures of Brain Degradation

8. Degradation cont’d

9. Senile Plaques
 Densely packed fibrous
structures called amyloid
bodies.
 Consists of mainly protein,
4-kDa peptide.
 Many isoforms make up
the amyloid proteins.
 Amyloid precursor protein
another source of which
can lead to AD. Functional
role unknown.

10. Neurofibrillary Tangles
 Consist of helical filaments called PHF.
 Intertwined protein strands made of tau protein
molecules.
 Formation of NFT’s not unique to AD.
 Found in many other neurodegenerative disorders with
dementias, affecting the brain.
 Scientists believe that the amyloid proteins lead to
the formation of the neurofibrillary tangles, and
both can lead to AD symptoms.

11. Diagnosis
 Only definitive way is to use brain scans (CT) to see
plaques or tangles in brain tissue.
 Tests used to exclude other diseases.

12. Treatments
 No treatment can prevent Alzheimer’s
 Drugs for early stages
 Cognax, Aricept, Exelon, or Razadyne
 Severe stages
 Memantine (Namenda)
 Medicines used to control symptoms, allow caregivers
to provide easier care.

13. Recent advances
 New therapeutics strategies for treatment of
Alzheimer's-
 Two classes of compounds-
 AChEIs and NMDA receptor blockers
 But with new addition e.g- neuroleptics and
serotonin modulating antidepressant effective
management of AD.

14. Research
 Neuroimaging
 Finding damaged parts of the brain
 Alzheimer’s Genetics
 Anti-oxidants
 Ginkgo biloba(age dependent spatial conginitive)
 Using to stimulate memory
 Estrogen
 Tested for levels found in AD patients, which are women

15. References
 Pasternak, J. Jack. Introduction to Molecular Genetics. 2nd
edition.2005. pg. 403-408.
 Recent advances in the neurobiology and
neuropharmacology of Alzheimer disease (article)-2017
 www.bic.ucs.edu/images/alz3d.jpg
 www.ahaf.org
 www.nia.nih.gov/Alzheimers/Publications