Alzheimer’s Disease

Alzheimer’s Disease

Q. 1

Alzheimer’s disease, which is involved ?

 A

Frontal cortex

 B

Cortical atrophy of temporoparietal cortex

 C

Frontal and parietal cortex

 D

Occipital cortex

Q. 1

Alzheimer’s disease, which is involved ?

 A

Frontal cortex

 B

Cortical atrophy of temporoparietal cortex

 C

Frontal and parietal cortex

 D

Occipital cortex

Ans. B

Explanation:

Cortical atrophy of temporoparietal cortex [Ref Robbins 7thle p 1386] Alzhiemer’s disease

Pathological features

The major pathological features in Alzhiemer’s disease are:-

  • Cerebral atrophy
  • Neuronal loss
  • Amyloid plaques
  • Neurofibrillary tangles

These changes are most severe in the following locations in decreasing order:

  • Medial temporal lobes

– Including the amygdala, hippocampal formation and entorhinal cortex.

  • Basal temporal cortex

Extending over the lateral posterior temporal cortex, parieto occipital cortex and posterior cingulate gyrus

  • Frontal lobes

– An important point is that primary motor, somatosensory, visual and auditory cortices are relatively spared


Q. 2 Which of the following is feature of Alzheimer’s disease
 A Early memory loss
 B Recent memory loss
 C Recent and past memory loss
 D Global memory loss
Q. 2 Which of the following is feature of Alzheimer’s disease
 A Early memory loss
 B Recent memory loss
 C Recent and past memory loss
 D Global memory loss
Ans. B

Explanation:

Recent memory loss


Q. 3

Degenerated neurofilaments seen in patients with Alzheimer’s disease are:

 A Hirano bodies
 B Lipofuscin granules
 C Neurofibrillary tangles
 D Amyloid plaques
Q. 3

Degenerated neurofilaments seen in patients with Alzheimer’s disease are:

 A Hirano bodies
 B Lipofuscin granules
 C Neurofibrillary tangles
 D Amyloid plaques
Ans. C

Explanation:

Neurofibrillary tangles


Q. 4 The following is not a feature of Alzheimer’s disease:
 A Neurofibrillary tangles
 B Senile (neurotic) plaques
 C Amyloid angiopathy
 D Lewy bodies
Q. 4 The following is not a feature of Alzheimer’s disease:
 A Neurofibrillary tangles
 B Senile (neurotic) plaques
 C Amyloid angiopathy
 D Lewy bodies
Ans. D

Explanation:

Lewy bodies


Q. 5

Which ONE feature could help to differenciate Alzheimer’s Dementia from Delirium in a 70 year old man with Urinary Tract Infection?

 A

Memory Disturbances

 B

Apraxia

 C

Delusion

 D

Delusion

Q. 5

Which ONE feature could help to differenciate Alzheimer’s Dementia from Delirium in a 70 year old man with Urinary Tract Infection?

 A

Memory Disturbances

 B

Apraxia

 C

Delusion

 D

Delusion

Ans. D

Explanation:

Delirium is broadly defined as an acute decline in attention and cognition.

It is characterized by altered sensorium, confusion, stupor, and fluctuations of consciousness.

 
Dementia is defined as a progressive impairment of cognitive functions occurring in clear consciousness (i.e. in the absence of delirium).

Q. 6

Neuritic plaques are associated with which of the following disease?

 A

Alzheimer’s disease

 B

Multiple sclerosis

 C

Stroke

 D

None of the above

Q. 6

Neuritic plaques are associated with which of the following disease?

 A

Alzheimer’s disease

 B

Multiple sclerosis

 C

Stroke

 D

None of the above

Ans. A

Explanation:

Neuritic plaques are associated with Alzheimer’s disease.
Neuritic plaques range in size from 20 to 200 μm in diameter; microglial cells and reactive astrocytes are present at their periphery.
Plaques are found in the hippocampus, amygdala, and neocortex, although there is usually relative sparing of primary motor and sensory cortices (this also applies to neurofibrillary tangles).
The amyloid core, which can be stained by Congo Red, contains several abnormal proteins. The dominant component of the amyloid plaque core is Aβ, a peptide derived through specific processing events from a larger molecule, amyloid precursor protein (APP).
           
Ref:
Robbins 8th edition Chapter 28.

Q. 7

Which chromosomal anomaly associated with alzheimer’s dementia?

 A

Trisomy 18

 B

Trisomy 21

 C

Patau syndrome.

 D

Turners syndrome

Q. 7

Which chromosomal anomaly associated with alzheimer’s dementia?

 A

Trisomy 18

 B

Trisomy 21

 C

Patau syndrome.

 D

Turners syndrome

Ans. B

Explanation:

Several genes play important pathogenic roles in at least some patients with Alzheimer’s disease(AD). One is the APP gene on chromosome 21. Adults with trisomy 21 (Down syndrome) consistently develop the typical neuropathologic hallmarks of AD if they survive beyond age 40. Presenilin-1 (PS-1) is on chromosome 14 and encodes a protein called S182. Mutations in this gene cause an early-onset AD transmitted in an autosomal dominant, highly penetrant fashion. The Apo E gene on chromosome 19 is involved in the pathogenesis of late-onset familial and sporadic forms of AD.

AD most often presents with an insidious onset of memory loss followed by a slowly progressive dementia over several years. Pathologically, atrophy is distributed throughout the medial temporal lobes, lateral and medial parietal lobes and lateral frontal cortex. Microscopically, there are neuritic plaques containing A-beta, neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau filaments, and accumulation of amyloid in blood vessel walls in cortex and leptomeninges.

Clinical Manifestation begins with memory impairment and spreading to language and visuospatial deficits.The management of AD is challenging and gratifying, despite the absence of a cure or a robust pharmacologic treatment. Donepezil (target dose, 10 mg daily), rivastigmine (target dose, 6 mg twice daily or 9.5-mg patch daily), galantamine (target dose 24 mg daily, extended-release), memantine (target dose, 10 mg twice daily), and tacrine are the drugs presently approved by the Food and Drug Administration (FDA) for treatment of AD.

Ref:Harrison’s Internal Medicine, 18th Edition, Pages 3307, 3309, 3049


Q. 8

The area of the brain resistant to Neurofibrillary tangles of Alzheimer’s disease is:

 A

Visual association areas

 B

Entorhinal cortex

 C

Temporal lobe

 D

Lateral geniculate body

Q. 8

The area of the brain resistant to Neurofibrillary tangles of Alzheimer’s disease is:

 A

Visual association areas

 B

Entorhinal cortex

 C

Temporal lobe

 D

Lateral geniculate body

Ans. D

Explanation:

Lateral geniculate body of the thalamus is resistant to the neurofibrillary tangles of Alzheimer’s disease. So lateral geniculate body is the single best answer of choice.

 
Ref: Harrisons Principles of Internal Medicine, 16th Edition, Pages 2398-2401.

 


Q. 9

Which of the following is used for treatment of Alzheimer’s disease?

 A

Donepezil

 B

Rivastigmine

 C

Galantamine

 D

All of the above

Q. 9

Which of the following is used for treatment of Alzheimer’s disease?

 A

Donepezil

 B

Rivastigmine

 C

Galantamine

 D

All of the above

Ans. D

Explanation:

Tacrine (tetrahydroaminoacridine, THA), a long-acting cholinesterase inhibitor and muscarinic modulator, was the first drug shown to have any benefit in Alzheimer’s disease. Because of its hepatic toxicity, tacrine has been almost completely replaced in clinical use by newer cholinesterase inhibitors: donepezil, rivastigmine, and galantamine.

These agents are orally active, have adequate penetration into the central nervous system, and are much less toxic than tacrine. Although evidence for the benefit of cholinesterase inhibitors (and memantine; see below) is statistically significant, the clinical benefit from these drugs is modest and temporary

 
Ref: Katzung 11th edition Chapter 60.

 


Q. 10

Protein involved in Alzheimer’s disease :

 A

Apo E gene

 B

Presel in – II

 C

Amyloid portion

 D

All

Q. 10

Protein involved in Alzheimer’s disease :

 A

Apo E gene

 B

Presel in – II

 C

Amyloid portion

 D

All

Ans. A

Explanation:

A i.e. Apo E gene


Q. 11

Biochemical etiology of Alzheimer’s disease relates it to :

 A

Acetylcholine

 B

GABA

 C

Serotinin

 D

Dopamine

Q. 11

Biochemical etiology of Alzheimer’s disease relates it to :

 A

Acetylcholine

 B

GABA

 C

Serotinin

 D

Dopamine

Ans. A

Explanation:

A i.e. Acetyl choline


Q. 12

Dementia of Alzheimer’s type is not associated with one of the following :

 A

Depressive symptoms

 B

Delusions

 C

Apraxia and aphasia

 D

Cerebral infarcts

Q. 12

Dementia of Alzheimer’s type is not associated with one of the following :

 A

Depressive symptoms

 B

Delusions

 C

Apraxia and aphasia

 D

Cerebral infarcts

Ans. D

Explanation:

D i.e.Cerebral infarcts


Q. 13

All the following are featuring Alzheimer’s disease except:

 A

Cerebellar atrophy

 B

Common in 5th and 6th decade

 C

Atrophied gyri widened sulci

 D

Peogressive dementia

Q. 13

All the following are featuring Alzheimer’s disease except:

 A

Cerebellar atrophy

 B

Common in 5th and 6th decade

 C

Atrophied gyri widened sulci

 D

Peogressive dementia

Ans. A

Explanation:

A i.e. Cerebellar atrophy


Q. 14

In Alzheimer’s disease (AD) which of the following is not seen:

 A

Aphasia

 B

Acalculia

 C

Agnosia

 D

Apraxia

Q. 14

In Alzheimer’s disease (AD) which of the following is not seen:

 A

Aphasia

 B

Acalculia

 C

Agnosia

 D

Apraxia

Ans. B

Explanation:

B i.e. Acalculia


Q. 15

False regarding Alzheimer’s disease (AD) is:

 A

Number of senile neural plaques correlates (increases) with age

 B

Presence of tau protein suggest neurodegeneration

 C

Number of neurofibrillary tangles is associated with the severity of dementia

 D

Extracellular inclusions (lesions) can occur in the absence of intracellular inclusions to make

Q. 15

False regarding Alzheimer’s disease (AD) is:

 A

Number of senile neural plaques correlates (increases) with age

 B

Presence of tau protein suggest neurodegeneration

 C

Number of neurofibrillary tangles is associated with the severity of dementia

 D

Extracellular inclusions (lesions) can occur in the absence of intracellular inclusions to make

Ans. D

Explanation:

D i.e. Extracellular inclusions (lesions) can occur in the absence of intracellular inclusions to make pathological diagnosis of AD

Characteristic cognitive impairments in Alzheimer’s disease include amnesia, aphasia, agnosia, and apraxia (the 4 As)Q. These four impairments are also included in DSM-IV TR diagnostic criteria of Alzheimer’s disease. However, there appears no cognitive functions that are truely preserved in AD. Visuo-spatial difficulties commonly occur in the middle stages of the disorder and may result in topographical disorientation, wandering and becoming lost. Difficulties with calculation (acalculia), attention and cognitive planning all occur.

–  For neuropathological diagnosis of AD, h/o dementia, extracellular neuritic senile (amyloid) plaques and intracellular NFTs all are required. Number of senile plaque increases with age, number of NFTs correlates with severity of dementia and presence of tau (r) protein suggest neurodegenerationQ.

It is the most common cause of dementiaQ. It causes gradually progressive cortical (parieto-temporal) dementiaQ beginning with memory impairment and spreading to language and visuospatial deficits over a prolonged courseQ.


Q. 16

Area of brain resistant to NFTs in Alzheimer’s disease:

 A

Visual association area

 B

Entorhinal cortex

 C

Lateral geniculate body

 D

Cuneal gyrus area VI / temporal lobe

Q. 16

Area of brain resistant to NFTs in Alzheimer’s disease:

 A

Visual association area

 B

Entorhinal cortex

 C

Lateral geniculate body

 D

Cuneal gyrus area VI / temporal lobe

Ans. C

Explanation:

C i.e. Lateral geniculate body

Alzheimer’s disease, a type of cortical dementia, does not involved sub cortical areas such as lateral geniculate body (nucleus)- a part of thalamusQ. Earliest and most severe degeneration is usually found in medial temporal lobe (entorhinal/ perirhinal cortex & hippocampus), lateral temporal cortex and nucleus basalis of MeynertQ. Area of visual association and cuneal gyrus (VI) are also cortical areas.


Q. 17

Regarding Alzheimer’s disease which is/are not true :

 A

Initial loss of long term memory

 B

Delayed loss of short term memory

 C

Step ladder pattern

 D

All

Q. 17

Regarding Alzheimer’s disease which is/are not true :

 A

Initial loss of long term memory

 B

Delayed loss of short term memory

 C

Step ladder pattern

 D

All

Ans. D

Explanation:

A. i.e. Initial loss of long term memory B. i.e. Delayed loss of short term memory C. i.e. Step ladder pattern


Q. 18

A/E are true regarding Alzheimer’s disease. 

 A

Gradually progressive

 B

Abrupt onset acute exacerbation

 C

Episodic memory

 D

All

Q. 18

A/E are true regarding Alzheimer’s disease. 

 A

Gradually progressive

 B

Abrupt onset acute exacerbation

 C

Episodic memory

 D

All

Ans. B

Explanation:

B i.e. Abrupt onset acute exacerbation


Q. 19

A 70 yr old man presents with 10 prosopagnosia loss of memory, 3rd person hallucination since 1 month. On examination deep Tendon reflexes are increased, minimental examination score is 20/30. What is most likely diagnosis:

 A

Dissociated Dementia

 B

Schizphrenia

 C

Alzheimers disease

 D

Psychotic disorder

Q. 19

A 70 yr old man presents with 10 prosopagnosia loss of memory, 3rd person hallucination since 1 month. On examination deep Tendon reflexes are increased, minimental examination score is 20/30. What is most likely diagnosis:

 A

Dissociated Dementia

 B

Schizphrenia

 C

Alzheimers disease

 D

Psychotic disorder

Ans. C

Explanation:

C i.e. Alzheimer’s disease

  • Duration of 1 month only, is enough to rule out schizophrenia, in which duration should be at least 6 months
  • In psychiatric disorders like schizophrenia & psychosis, there may never be organic symptoms like increased tendon reflexes.
  • Features of Alzheimer dementia are
  1. Memory impairment without impairment of consciousnessQ
  2. AgnosognosiaQ (Unware of his problem) Prosopangosia (difficulty in identifying known faces)
  3. Focal neurological signs (ex assymetrical hyper-reflexia or weakness)Q
  4. Primitive reflexes (ex grasp, snout, suck, palmo-mental, & tonic foot reflexes)
  5. Frontal lobe signs
  6. Aphasia (language disturbance)
  7. Apraxia (impaired ability to carry out motor activities despite intact motor function)
  8. Agnosia (failure to recognize or identify objects despite intact sensory function)
  9. Disturbance in executive functioning (i.e. planning, organizing, sequencing, abstracting)

Q. 20

Biochemical etiology of Alzheimer’s disease relates to

 A

Serotonin

 B

Dopamine

 C

Acetyl choline

 D

GABA

Q. 20

Biochemical etiology of Alzheimer’s disease relates to

 A

Serotonin

 B

Dopamine

 C

Acetyl choline

 D

GABA

Ans. C

Explanation:

C i.e. Acetyl choline

Disease

Related Neurotransmitter

Alzheimer’s disease

Acetyl cholineQ & Nor epinephrine are hypoactive

–    So anticholine-esterase – TacrineQ is used in treatment

Depression

Norepinephrine, Serotonin (5-HT)Q & Dopamine are reduced

OCN/Suicide

Serotonin (5 HT)Q

Schizophrenia

Dopamine, Serotonin & Norepinephrine are tedQ


Q. 21

In Alzheimer disease, seen are:        

 A

Neurofibrillary tangles

 B

Neuritic plaques

 C

Pick’s protein

 D

a and b

Q. 21

In Alzheimer disease, seen are:        

 A

Neurofibrillary tangles

 B

Neuritic plaques

 C

Pick’s protein

 D

a and b

Ans. D

Explanation:

Ans. is ‘a’ i.e., Neurofibrillary tangles; ‘b’ i.e.,Neuritic plaques


Q. 22

In Alzheimer’s disease, the pathology seen in the brain is –

 A

Atrophy of parietal and temporal lobes

 B

Atrophy of parietal and temporal lobes

 C

Atrophy of temporal and occipital lobes

 D

Atrophy of parietal and occipital lobes

Q. 22

In Alzheimer’s disease, the pathology seen in the brain is –

 A

Atrophy of parietal and temporal lobes

 B

Atrophy of parietal and temporal lobes

 C

Atrophy of temporal and occipital lobes

 D

Atrophy of parietal and occipital lobes

Ans. A

Explanation:

Ans. is ‘a’ i.e., Atrophy of parietal and temporal lobes

Gross pathology in Alzhiemer’s disease:

o Diffuse cerebral atrophy of the hippocampus, amygdala and entorhinal cortex.

o Enlargement of the ventricles caused by neuronal loss.

  • Grossly the brain shows a variable degree of cortical atrophy marked by widening of the cerebral sulci.
  • These changes are most pronounced in the temporal and parietal lobes:

 Frontal lobes can also be involved.


Q. 23

The fixative used in histopathology ‑

 A

10% buffered neutral formalin

 B

Bouins fixative

 C

Glutaraldehyde

 D

Ethyl alcohol

Q. 23

The fixative used in histopathology ‑

 A

10% buffered neutral formalin

 B

Bouins fixative

 C

Glutaraldehyde

 D

Ethyl alcohol

Ans. A

Explanation:

Ans. is ‘a’ 10% buffered neutral formalin


Q. 24

Donepezil is used in the treatment of which of the following conditions –

 A

Schizophrenia

 B

Depression

 C

Anxiety

 D

Alzheimer dementia

Q. 24

Donepezil is used in the treatment of which of the following conditions –

 A

Schizophrenia

 B

Depression

 C

Anxiety

 D

Alzheimer dementia

Ans. D

Explanation:

Ans. is ‘d’ i.e., Alzheimer disease

o Donepezil is a cerebroactive drug. It is used in Alzheimer’s disease (AD).


Q. 25

Galantamine is used in ?

 A

Alzheimer’s disease

 B

Parkinson’s disease

 C

Emesis

 D

Chorea

Q. 25

Galantamine is used in ?

 A

Alzheimer’s disease

 B

Parkinson’s disease

 C

Emesis

 D

Chorea

Ans. A

Explanation:

Ans. is ‘a’ i.e., Alzheimer’s diseaes


Q. 26

A patient of Alzheimer’s disease is on rivastigmine therapy and develops symptoms of depression. Use of which of the following drug would decrease efficacy of rivostigmine –

 A

TCAs

 B

SSRI

 C

MAO inhibitor

 D

RIMA

Q. 26

A patient of Alzheimer’s disease is on rivastigmine therapy and develops symptoms of depression. Use of which of the following drug would decrease efficacy of rivostigmine –

 A

TCAs

 B

SSRI

 C

MAO inhibitor

 D

RIMA

Ans. A

Explanation:

Ans. is ‘a’ i.e., TCAs

o Cholinergic transmission is diminished in Alzheimer’s disease.

o All agents that benefit the conduction act to enhance acetyhcholine activity by inhibition of the acetylcholinesterase which metabolises and inactivates acetylcholine.

o Consequently acetylcholine remains usable for longer.

o Rivastigmine acts in similar way.

o Tricyclic antidepressants (TCAs) have anticholinergic property, therefore they counteract that cholinergic effect of rivastigmine.


Q. 27

Which of the following drugs should not be used with rivastigmine in patients with alzheimer’s disease –

 A

SSRI

 B

Tricyclic antidepressant

 C

RIMA

 D

Atypical antidepressants

Q. 27

Which of the following drugs should not be used with rivastigmine in patients with alzheimer’s disease –

 A

SSRI

 B

Tricyclic antidepressant

 C

RIMA

 D

Atypical antidepressants

Ans. B

Explanation:

Ans. is ‘b’ i.e., Tricyclic antidepressant

Rivastigmine (cholinesterase inhibitor) should not be used with drugs that have cholinergic antagonistic activity like tricyclic antidepressants (TCA) as the combination is counter productive.


Q. 28

A chromosomal anomaly associated with Alzheimer’s dementia is:

 A

Trisomy 18

 B

Patau syndrome

 C

Trisomy 21

 D

Turners syndrome

Q. 28

A chromosomal anomaly associated with Alzheimer’s dementia is:

 A

Trisomy 18

 B

Patau syndrome

 C

Trisomy 21

 D

Turners syndrome

Ans. C

Explanation:

Answer is C (Trisomy 21) :

Several genetic factors are known to play important roles in pathogenesis of at least some cases of Alzheimers disease. Trisomy 21 is one of them.

Adults with trisomy 21 (Down’s) consistently develop the Neuropathologic hallmark’s of Alzheimer’s disease if they survive beyond age 40.


Q. 29

Which of the following is predominantly involved in Alzheimer’s dementia:

 A

Frontal cortex

 B

Temporo-Parietal cortex

 C

Fronto-Parietal cortex

 D

Franto-Temporal cortex

Q. 29

Which of the following is predominantly involved in Alzheimer’s dementia:

 A

Frontal cortex

 B

Temporo-Parietal cortex

 C

Fronto-Parietal cortex

 D

Franto-Temporal cortex

Ans. B

Explanation:

Answer is B (Temporo-Parietal cortex):

Alzheimer’s disease predominantly affects the temporoparietal cortex although frontal lobe is also frequently involved

Alzheimer’s disease predominantly affects the temporo-parietal cortex’ – Alzheimer’s Disease by Terry Regional deficits are most prominent in the temporo-parietal cortex’ – Alzheimer’s Disease by Terry


Q. 30

All of the following are known predisposing factors for Alzheimer’s disease except :

 A

Down-syndrome

 B

Low education level

 C

Smoking

 D

Female sex

Q. 30

All of the following are known predisposing factors for Alzheimer’s disease except :

 A

Down-syndrome

 B

Low education level

 C

Smoking

 D

Female sex

Ans. C

Explanation:

Answer is C (Smoking):

Smoking has not been mentioned as a risk factor, for Alzheimer’s disease.


Q. 31

All of the following neurotransmitter deficiencies are observed in Alzheimer’s disease, Except

 A

Acetylcholine

 B

Serotonine

 C

Noradrenaline

 D

Dopamine

Q. 31

All of the following neurotransmitter deficiencies are observed in Alzheimer’s disease, Except

 A

Acetylcholine

 B

Serotonine

 C

Noradrenaline

 D

Dopamine

Ans. D

Explanation:

Answer is D (Dopamine):

Dopamine deficiency is not a feature of Alzheimer’s disease.


Q. 32

Which of the following is the most important neurotransmitter deficient in the cortex of patients with Alzheimer’s Disease

 A

Acetylcholine

 B

Serotonin

 C

Dopamine

 D

Noradrenaline

Q. 32

Which of the following is the most important neurotransmitter deficient in the cortex of patients with Alzheimer’s Disease

 A

Acetylcholine

 B

Serotonin

 C

Dopamine

 D

Noradrenaline

Ans. A

Explanation:

Answer is A (Acetylcholine):

The most important biochemical abnormality in Alzheimer’s disease is the decrease in cortical levels of Acetylcholine

Biochemically Alzheimer’s disease is associated with a decrease in the cortical levels of several proteins and neurotransmitters especially acetylcholine, its synthetic enzyme choline-acetyl-transferase, and nicotinic cholinergic receptors. Reduction of acetylcholine is related in part to degeneration of cholinergic neurons in the nucleus basalis of Meynert (NBM) that projects through the cortex. There is also noradrenergic and serotonergic depletion due to degeneration of brainstem nuclei such as the locus ceruleus and dorsal raphe’ – Harrison’s


Q. 33

Alzheimer’s Disease is associated with :

 A

Delerium

 B

Delusion

 C

Dementia

 D

Depression

Q. 33

Alzheimer’s Disease is associated with :

 A

Delerium

 B

Delusion

 C

Dementia

 D

Depression

Ans. C

Explanation:

Answer is C (Dementia):

Alzheimer’s Disease is the most common cause of Dementia in elderly.

Clinically, AD most often presents with subtle onset of memory loss followed by slowly progressive dementia that has a course of several years.


Q. 34

Which of the following is not seen in early onset Alzheimer’s Disease:

 A

Aphasia

 B

Apraxia

 C

Acalculia

 D

None

Q. 34

Which of the following is not seen in early onset Alzheimer’s Disease:

 A

Aphasia

 B

Apraxia

 C

Acalculia

 D

None

Ans. D

Explanation:

Answer is None (All are seen) > Agnosia

Aphasia, Apraxia, Acalculia and Agnosias may all be seen in Alzheimer’s Dementia.

`Agnosia’ in Alzheimer’s disease usually presents late in the disease and is not included in the ICD-10 Diagnostic criteria for dementia in Alzheimer’s disease with early onset and hence may be selected as the single best answer by exclusion.

Dementia in Alzheimer’s Disease with Early Onset (ICD-10 criterion)

  1. The criteria for dementia in Alzheimer’s Disease must be met, and the age at onset must be less than 65 years.
  2. In addition atleast one of the following requirements must be met:

a)     evidence of relatively rapid onset and progression

b)     in addition to memory impairment there must be:

Aphasia (Amnesia or sensory)

– Agraphia

–  Alexia (indicating the presence of temporal, parietal or frontal lobe involvement)

–  Acalculia or

–  Apraxia


Q. 35

Which of the following statements about the pathology in Alzheimer’s disease is not true:

 A

Neuritic Plaques are formed of amyloid protein

 B

Neurofibrillary tangles (NFT) are made of tau protein

 C

NFTs appear extracellularly before intracellular appearance

 D

Number of NFTs correlates with dementia

Q. 35

Which of the following statements about the pathology in Alzheimer’s disease is not true:

 A

Neuritic Plaques are formed of amyloid protein

 B

Neurofibrillary tangles (NFT) are made of tau protein

 C

NFTs appear extracellularly before intracellular appearance

 D

Number of NFTs correlates with dementia

Ans. C

Explanation:

Answer is C (NFTs appear extracellularly before intracellular appearance):

NFTs are typically seen intracellularly within the soma and proximal dendrites of neurons.

Neurofibrillary Tangles (NFTs) are intracellular accumulations of hyperphosphorylated ‘tau’ proteins.

Neurofibrillary Tangles are Intracellular Accumulations

  • Neurofibrillary Tangles are intracellular accumulations of hyperphosphorylated microtubule binding protein ‘tau’.
  • Paired helical filaments of tau protein (NFTs) form intracellularly within the soma and proximal dendrites of neurons.
  • These cytoskeletal protein tangles (NFTs), initially impede cellular metabolism and axosplasmic transport leading to impaired synaptic function and eventually to neuronal death.
  • These neurofibrillaty tangles may be seen as extracellular tangles after degeneration of the neuron as evidence of the neuronal cell’s demise
  • Neurofibrillary Tangles are intracellular accumulations that may appear extracellularly alter degeneration of neuron (neuronal death)

Histopathological Hallmarks of Alzheimer’s Disease

Amyloid Plaques (Extracellular)

  • Amyloid Neuritic Plaques are formed by extracellular accumulation of beta amyloid deposits within the neutropil
  • ‘Neuritic’ or ‘Senile’ I3-amyloid plaques are an early histopathological sign of Alzheimer’s disease (that occur rarely in healthy subjects)
  • The amyloid 13-protein accumulated in single neuritic plaques is toxic to surrounding structures and adjacent neurons.
  • Clinicopathological studies have shown that amy/aid burden does not directly correlate with severity or duration of dementia.

Neurofibrillary Tangles (Intracellular)

  • Neurofibrillary tangles arc formed by intracellular accumulation of hyperphosphorylated microtubule binding protein ‘tau’.
  • NFT’s occur in many neurodegenerative diseases and /or a group of diseases called laupathies’.
  • These include Frontotemporal dementia, Pick’s disease etc. The cooccurance of fi-amyloid plaques with NFT’s suggests a diagnosis of AD.
  • The NFT’s are toxic to the neurons and neurons with NFT’s eventually die and degenerate leaving a residual `ghost tangle’, in the extracellular space reminding of the pyramidal cell body in which it was initially formed.
  • Clinicopathological studies have shown that dementia correlates more strongly with NFT’s than with senile plaques (3-amyloid)

Q. 36

Which of the following areas of brain is most resistant to Neurofibrillary tangles in Alzheimer’s disease

 A

Entorhinal cortex

 B

Hippocampus /Temporal lobe

 C

Lateral Geniculate Body

 D

Visual Association area

Q. 36

Which of the following areas of brain is most resistant to Neurofibrillary tangles in Alzheimer’s disease

 A

Entorhinal cortex

 B

Hippocampus /Temporal lobe

 C

Lateral Geniculate Body

 D

Visual Association area

Ans. C

Explanation:

Answer is C (Lateral Geniculate Body):

The topographical and neuroanatomical distribution of Neurofibrillary tangles and Neuritic Plaques in the Cerebral cortex of patients with Alzheimer’s Disease’

– Cerebral Cortex (1991): (1): 103-116

`Lateral geniculate body’ is the least commonly affected area amongst the options provided.

Weurofibrillaiy tangles are region specific occuring predominantly in the Hippocampus, Entorhinal cortex and association areas of the Neocortex

‘The Neuropathology of Dementia’ (Cambridge) 1997/7

`Not even a single neuron with Neurofibrillary Tangles (NFT) was seen in the Lateral Geniculate Bodies’

Distribution of Alzheimer’s Neurofibrillary tangles (Taken from ‘Alzheimer’s Disease’ by George Parry (2006)/55)

Neuro fibrillary Tangles (NFT): Density distribution in Alzheimer’s disease

  • Entorhinal cortex — Hippocampus — Amygdala interconnections (most vulnerable)
  • Limbic and Temporal cortical areas (next most severely involved)
  • Association areas of the neocortex

Topographical Distribution of NFTs in Alzheimer’s disease

`The spatiotemporal pattern of progression of NFTs in Alzheimer’s disease is steriotypical and predictable.

Briefly, the neurofibrillary degeneration starts in the aliocortex of medial temporal lobe (entorhinal cortex and hippocampus) and spreads to the associative neocortex, relatively sparing the primary sensory and primary motor and visual cortex.’

Enterohinal cortex, Hippocampus and Associative areas of neocortex are primarily involved.

Taken from ‘Neuropathological Alterations in Alzheimer’s Disease’: Perspectives in Medicine 2011

Braak and Braak distinguished six stages to explain topographical distribution and progression of NFT.

Stage I

  • The first NFTs consistently appear in the Transentorhinal (perihilar) region along with Entorhinal cortex proper

Stage II

  • NFTs appear in the CA I region of the Hippocampus

Stage III

  • NFTs appear in the Limbic structures such as the subiculum of H ppocampal formation

Stage IV

  • NFTs appear in the Amygdala, Thalamus & Claustrum

Stage V

  • NFTs appear in all isocortical areas with the affection of Associative areas

Stage VI

NFTs appear in primary sensory, motor and visual areas (Primary sensory, motor and visual area are considered most resistant)

These six stages can be summarized into three for the purpose of understanding, namely: Entorhinal, Limbic and isocortical


Q. 37

The following is not a feature of Alzheimer’s disease:

 A

Neurofibrillary tangles

 B

Senile (neuritic) plaques

 C

Amyloid Angiopathy

 D

Lewy bodies

Q. 37

The following is not a feature of Alzheimer’s disease:

 A

Neurofibrillary tangles

 B

Senile (neuritic) plaques

 C

Amyloid Angiopathy

 D

Lewy bodies

Ans. D

Explanation:

Answer is D (Lewy bodies):

Lew), bodies’ are characteristically seen in idiopathic parkinsons disease (and not in Alzheimer’s disease).

Alzheimer’s disease is the most common cause of dementia in the Western world and is characterized by the following clinical, pathological and biochemical triad.


Q. 38

Amongst the following cause of dementia, neurofibrillary tangles, senile plaques and amyloid angiopathy are associated with:               

September 2003

 A

Creutzfeldt-Jacob disease

 B

Vascular dementia

 C

Niemann Pick disease

 D

Alzheimer’s disease

Q. 38

Amongst the following cause of dementia, neurofibrillary tangles, senile plaques and amyloid angiopathy are associated with:               

September 2003

 A

Creutzfeldt-Jacob disease

 B

Vascular dementia

 C

Niemann Pick disease

 D

Alzheimer’s disease

Ans. D

Explanation:

Ans. D i.e. Alzheimer’s disease


Q. 39

Neurofibrillary tangles are associated with:

March 2007

 A

Bipolar disorder

 B

Alzheimer’s disease

 C

Schizophrenia

 D

Multiple infarctions

Q. 39

Neurofibrillary tangles are associated with:

March 2007

 A

Bipolar disorder

 B

Alzheimer’s disease

 C

Schizophrenia

 D

Multiple infarctions

Ans. B

Explanation:

Ans. B: Alzheimer’s Disease

Neurofibrillary tangles were first described by Alois Alzheimer in one of his patients suffering from the disorder now referred to as Alzheimer’s disease.

Neurofibrillary tangles are pathological protein aggregates found within neurons in cases of Alzheimer’s disease. Tangles are formed by hyperphosphorylation of a microtubule-associated protein known as tau, causing it to aggregate in an insoluble form. (These aggregations of hyperphosphorylated tau protein are also referred to as PHF, or “Paired Helical Filaments”).

It is also believed that neurofibrillary tangles are seen in Creutzfeldt-Jakob disease.

Neurofibrillary tangles are also found in Supranuclear palsy.

It’s also related to frontotemporal dementia however without detectable (beta}-amyloid plaques.


Q. 40

Which of the following is not a pathological find­ing seen in alzheimer’s disease ‑

 A

Cortical atrophy

 B

Neurofibrillary tangles

 C

Neuritic plaques

 D

Lewy body

Q. 40

Which of the following is not a pathological find­ing seen in alzheimer’s disease ‑

 A

Cortical atrophy

 B

Neurofibrillary tangles

 C

Neuritic plaques

 D

Lewy body

Ans. D

Explanation:

Ans. is ‘d’ i.e., Lewy body


Q. 41

Neurotransmitter playing major part in the pathogenesis of Alzheimer’s disease ‑

 A

Serotonine

 B

Norepinephrine

 C

Acetylcholine

 D

Dopamine

Q. 41

Neurotransmitter playing major part in the pathogenesis of Alzheimer’s disease ‑

 A

Serotonine

 B

Norepinephrine

 C

Acetylcholine

 D

Dopamine

Ans. C

Explanation:

Ans. is ‘c’ i.e., Acetylcholine

Neurotransmitters in Alzheimer’s disease

  • Acetylcholine has a major role in memory functions and deficiency in cholinergic functioning is associatedwith memory disturbances particularly short term memory. In Alzheimer’s disease there loss of cells in the nucleus basalis of meyernet results in marked reduction in choline acetyltransferase (CHAT), an enzymeinvolved in the synthesis of acetylcholine —> Decreased Acetylcholine.
  • The other important neurotransmitter involved is norepinephrine —> There is decrease in nor-epinephrine containing neurons in the locus ceruleus.
  • Two other neuroactive peptides have been implicated in AD —> Somatostatin and corticotropin, both of which have decreased concentration.


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