Alzheimer’s Disease: Symptoms, Causes and Treatment

Alzheimer’s disease is the leading cause of cortical or senile dementia. It can manifest as early as in the third decade of life and presents with loss of episodic memory followed by slowly progressive dementia. The Alzheimer’s disease patient needs regular care and the emotional toll for family members and caregivers is immeasurable. The development in medical science is opening the door to early detection and management of Alzheimer's disease with biologically specific therapies.

Causes Of Alzheimer’s Disease

• Several genes play an important role in the pathogenesis of Alzheimer’s disease.
• It has been found that defects of chromosomes 1, 14, 19, and 21.
  • In chromosome 1, the Presenilin 2 gene is defective.
  • In chromosome 14, the Presenilin 1 gene is defective.
  • In chromosome 19, the ApoE gene is defective. The ApoE4 allele has a higher risk of developing Alzheimer’s disease whereas the ApoE2 allele has a lower risk.
  • In chromosome 21, the amyloid precursor protein is defective, and pre-senile dementia occurs at 35 years of age.

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Pathophysiology Of Alzheimer’s Disease

• The earliest and most severe degeneration in Alzheimer's disease patients is found in the medial temporal lobe, inferolateral temporal cortex, and nucleus of Meynert.
• The characteristic feature or finding of Alzheimer's disease is neuritic plaques of A beta Amyloid proteins and Neurofibrillary Tangles.
• The hyperphosphorylated Tau protein interferes with microtubule assembly and causes the formation of neurofibrillary tangles.
• These oligomers have been found to cause cellular dysfunction and toxicity.
• Alzheimer’s disease is found to be associated with a decrease in the level of neurotransmitters mainly acetylcholine which occurs due to degeneration of cholinergic neurons in the nucleus basalis of Meynert.
• There is also a depletion of nor-epinephrine and serotonin levels due to the degeneration of locus coeruleus and dorsal raphe respectively.
• Mainly parietal and temporal lobes are affected.

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Preclinical Alzheimer’s Disease

CSF PET biomarkers evidence is present in the absence of clinical features of Alzheimer's disease. These evidences are:

• A beta-amyloid deposition is seen.
• Amyloid in PET
• Tau in PET

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Clinical Features Of Alzheimer’s Disease

Mnemonic 4A is used to describe the clinical features of Alzheimer’s Disease:

Amnesia

• The patient will not be able to keep track of finances, will not be able to follow instructions, can’t drive, and can’t do shopping.
• The patient will not be able to do well socially.

Aphasia

• The patient’s ability to name someone will be hampered first.
• Loss of comprehension ability
• Then the patient will lose fluency in speech.

Apraxia

• There will be a loss of visual-spatial skills and it is diagnosed by a clock face test.
• Patients will not be able to use utensils and dressing will be improper.

Anosognosia

• The patient will be unaware of their neurological deficit and this condition makes them very vulnerable hence utmost care is required.
• There will be disinhibition, mutism, and shuffling gate will be seen in later stages.

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Diagnosis Of Alzheimer’s Disease/Workup

• Mini-mental state examination- it is done for the diagnosis of dementia.
  • For the screening test the cutoff score is <24/30. 
  • Mild dementia- 21-24
  • Moderate dementia - 10-20
  • Severe dementia - <10
• FBG glucose PET
  • Amyloid PET
  • Tau PET
  • CSF A-beta 42 will be lower in levels.
• The investigation of choice is functional MRI. One functional MRI parietal and temporal activity will be observed reduced.
• On MRI, the blunting of gyrus/ sulcus to rule out frontotemporal cortex.
• Patients working memory is checked.
• Patient’s episodic memory is checked by asking patient for three word recall.
  • Attention calculation
  • Language comprehension
  • Figure copying is checked

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Treatment Of Alzheimer’s Disease

• Aducanumab- it is given intravenously for 4 weeks. It is used in early dementia. It binds to A beta amyloid.
• Donepezil
• Rivastigmine and Galantamine
• Tacrine
• The physician should build rapport with the patient, family members and the caregivers. Regular counseling of the patient and caregivers should be provided to avoid any emotional breakdown.

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