The role of amyloid $beta;-protein in Alzheimer's disease

Regland, Björn; Gottfries, C. G.

doi:10.1016/0140-6736(92)91780-c

Cited by 64 publications

(50 citation statements)

References 29 publications

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“…This conclusion is supported by the localisation of several acute-phase proteins within the different morphological types of Aβ deposit including diffuse, primitive, and classic deposits, e.g., amyloid-P, complement factors, and a-antichymotrypsin [7] ( Table I). Furthermore, Regland and Gottfries [108] proposed that APP is involved in AD secondarily to maintain cell function. APP may therefore, maintain neuronal growth and survival and its putative neurotrophic action is also suggested by the observation that it shares structural features with the precursor for epidermal growth factor [108].…”

Section: Correlation Of Classical Pathology With Clinical Dementiamentioning

confidence: 99%

“…Furthermore, Regland and Gottfries [108] proposed that APP is involved in AD secondarily to maintain cell function. APP may therefore, maintain neuronal growth and survival and its putative neurotrophic action is also suggested by the observation that it shares structural features with the precursor for epidermal growth factor [108]. Furthermore, NFT may be part of the neurons response to injury [109].…”

Section: Correlation Of Classical Pathology With Clinical Dementiamentioning

confidence: 99%

“…The brain is the ultimate mediator of stress-related mortality through hormonal changes resulting in hypertension, glucose intolerance, cardiovascular disease, and immunological problems [25]. Second, the consequence of increasing allostatic load is gradual synaptic disconnection, neuronal degeneration, and the upregulation of genes determining various reactive and breakdown products resulting in the formation of Aβ and tau [14,96,108,138]. Third, in small numbers of families, specific APP or PSEN mutations influence the outcome of this age-related degeneration by determining the quantity, solubility, and/or toxicity of the molecular product.…”

Section: Genetic Risk Factors (Apo E)mentioning

confidence: 99%

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A critical analysis of the ‘amyloid cascade hypothesis’

Armstrong¹

2014

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A b s t r a c t The 'amyloid cascade hypothesis' (ACH) is the most influential model of the pathogenesis of Alzheimer's disease (AD). The hypothesis proposes that the deposition of β-amyloid (Aβ) is the initial pathological event in AD, leading to the formation of extracellular senile plaques (SP), tau-immunoreactive neurofibrillary tangles (NFT), neuronal loss, and ultimately, clinical dementia. Ever since the formulation of the ACH, however, there have been questions regarding whether it completely describes AD pathogenesis. This review critically examines various aspects of the ACH including its origin and development, the role of amyloid precursor protein (APP), whether SP and NFT are related to the development of clinical dementia, whether Aβ and tau are 'reactive' proteins, and whether there is a pathogenic relationship between SP and NFT. The results of transgenic experiments and treatments for AD designed on the basis of the ACH are also reviewed. It was concluded: (1) Aβ and tau could be the products rather than the cause of neurodegeneration in AD, (2) it is doubtful whether there is a direct causal link between Aβ and tau, and (3) SP and NFT may not be directly related to the development of dementia, (4) transgenic models involving

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Section: Correlation Of Classical Pathology With Clinical Dementiamentioning

confidence: 99%

Section: Correlation Of Classical Pathology With Clinical Dementiamentioning

confidence: 99%

Section: Genetic Risk Factors (Apo E)mentioning

confidence: 99%

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A critical analysis of the ‘amyloid cascade hypothesis’

Armstrong¹

2014

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“…Several acute phase proteins are localised within Ab deposits in AD including amyloid-P, complement factors, and a-antichymotrypsin [98]. Furthermore, Regland and Gottfries [154] proposed that APP maintains cell function by supporting neuronal growth and survival. The possible neurotrophic action of APP is supported by the observation that it shares structural features with the precursor for the epidermal growth factor [154].…”

Section: Head Injurymentioning

confidence: 99%

“…Furthermore, Regland and Gottfries [154] proposed that APP maintains cell function by supporting neuronal growth and survival. The possible neurotrophic action of APP is supported by the observation that it shares structural features with the precursor for the epidermal growth factor [154]. NFT may also be a part of the neurons response to injury [205].…”

Section: Head Injurymentioning

confidence: 99%

Review article What causes alzheimer’s disease?

Armstrong¹

2013

177

119

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A b s t r a c t Since the earliest descriptions of Alzheimer's disease (AD), many theories have been advanced as to its cause. These include: (1) exacerbation of aging, (2) degeneration of anatomical pathways, including the cholinergic and cortico-cortical pathways, (3) an environmental factor such as exposure to aluminium, head injury, or malnutrition, (4) genetic factors including mutations of amyloid precursor protein (APP) and presenilin (PSEN) genes and allelic variation in apolipoprotein E (Apo E), (5) mitochondrial dysfunction, (6) a compromised blood brain barrier, (7) immune system dysfunction, and (8) infectious agents. This review discusses the evidence for and against each of these theories and concludes that AD is a multifactorial disorder in which genetic and environmental risk factors interact to increase the rate of normal aging ('allostatic load'). The consequent degeneration of neurons and blood vessels results in the formation of abnormally aggregated 'reactive' proteins such as b-amyloid (Ab) and tau. Gene mutations influence the outcome of age-related neuronal degeneration to cause early onset familial AD (EO-FAD

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Current pharmacological strategies in Alzheimer's disease

Kelly

Hunter

1995

Int J Geriat Psychiatry

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The role of amyloid $beta;-protein in Alzheimer's disease

Cited by 64 publications

References 29 publications

A critical analysis of the ‘amyloid cascade hypothesis’

A critical analysis of the ‘amyloid cascade hypothesis’

Review article What causes alzheimer’s disease?

Current pharmacological strategies in Alzheimer's disease

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