Precautions in Familial Transmissible Dementia

Cook, Robert H.; Austin, James H.

doi:10.1001/archneur.1978.00500350001001

Cited by 5 publications

(1 citation statement)

References 11 publications

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“…The enigmatic nature of Alzheimer's disease and this vignette surfaces for discussion the question about the etiology of this illness. Some studies support a genetic diathesis; 2 another theory suggests a viral etiology 3 . An association between Alzheimer's disease and toxic aluminum levels, 4 and an immunologic deficiency are also proposed 5 …”

Section: Discussionmentioning

confidence: 99%

Presumed Alzheimer's Disease Beginning at Different Ages in Two Twins

Embry

Lippmann

1985

J American Geriatrics Society

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Alzheimer's disease is a condition of gradually declining mental capacity with onset in the senium or pre-senium. This deinenting process is heralded by a progressive loss of memory for recent events. Clinical features include not only memory impairment but disorientation, decreased concentration, and often also anxiety, delusions, hallucinations, personality change, and neuromuscular disorders. A presumptive diagnosis of Alzheimer's disease is based on typical clinical and laboratory findings, but the diagnosis is definitive only with histologic confirmation of characteristic findings, such as senile plaques and neurofibrillary tangles. Etiology is unknown; various genetic, viral, toxic, and defective immune system theories have been advanced.This case depicts a patient with a presumptive diagnosis of Alzheimer's disease that began at 74 years of age. Her twin sister had a similar clinical picture beginning at age 68.

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Section: Discussionmentioning

confidence: 99%

Presumed Alzheimer's Disease Beginning at Different Ages in Two Twins

Embry

Lippmann

1985

J American Geriatrics Society

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Hypersensitivity to DNA-Damaging Agents in Abiotrophies: A New Explanation for Degeneration of Neurons, Photoreceptors, and Muscle in Alzheimer, Parkinson and Huntington Diseases, Retinitis Pigmentosa, and Duchenne Muscular Dystrophy

Robbins

Brumback

Polinsky

et al. 1985

Molecular Biology of Aging

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Binding between Prion Protein and Aβ Oligomers Contributes to the Pathogenesis of Alzheimer’s Disease

et al. 2019

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A plethora of evidence suggests that protein misfolding and aggregation are underlying mechanisms of various neurodegenerative diseases, such as prion diseases and Alzheimer's disease (AD). Like prion diseases, AD has been considered as an infectious disease in the past decades as it shows strain specificity and transmission potential. Although it remains elusive how protein aggregation leads to AD, it is becoming clear that cellular prion protein (PrP C ) plays an important role in AD pathogenesis. Here, we briefly reviewed AD pathogenesis and focused on recent progresses how PrP C contributed to AD development. In addition, we proposed a potential mechanism to explain why infectious agents, such as viruses, conduce AD pathogenesis. Microbe infections cause Ab deposition and upregulation of PrP C , which lead to high affinity binding between Ab oligomers and PrP C . The interaction between PrP C and Ab oligomers in turn activates the Fyn signaling cascade, resulting in neuron death in the central nervous system (CNS). Thus, silencing PrP C expression may turn out be an effective treatment for PrP C dependent AD.

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Precautions in Familial Transmissible Dementia

Cited by 5 publications

References 11 publications

Presumed Alzheimer's Disease Beginning at Different Ages in Two Twins

Presumed Alzheimer's Disease Beginning at Different Ages in Two Twins

Hypersensitivity to DNA-Damaging Agents in Abiotrophies: A New Explanation for Degeneration of Neurons, Photoreceptors, and Muscle in Alzheimer, Parkinson and Huntington Diseases, Retinitis Pigmentosa, and Duchenne Muscular Dystrophy

Binding between Prion Protein and Aβ Oligomers Contributes to the Pathogenesis of Alzheimer’s Disease

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