Senile‐Presenile Dementia: Follow‐Up Data on an Effective Psychotherapy‐Anticoagulant Regimen*

Walsh, Arthur C.; Walsh, Bernice H.; Melaney, Catherine

doi:10.1111/j.1532-5415.1978.tb03326.x

Cited by 54 publications

(15 citation statements)

References 5 publications

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“…This phenomenon has also been reported by Ahn and coworkers who showed that fibrin clots formed in the presence of Aβ have an abnormal structure, making them resistant to degradation [61]. In addition, anticoagulant treatment improves cognition in mouse models and of AD and dementia patients [29,[62][63][64]. However, anticoagulant therapy might cause severe problems in elderly patients having a fragile vasculature increasing the risk of systemic bleeding.…”

Section: Discussionsupporting

confidence: 69%

The blood clotting Factor XIIIa forms unique complexes with amyloid‐beta (Aβ) and colocalizes with deposited Aβ in cerebral amyloid angiopathy

Jager

Boot

Bol

et al. 2015

Neuropathology Appl Neurobio

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Section: Discussionsupporting

confidence: 69%

The blood clotting Factor XIIIa forms unique complexes with amyloid‐beta (Aβ) and colocalizes with deposited Aβ in cerebral amyloid angiopathy

Jager

Boot

Bol

et al. 2015

Neuropathology Appl Neurobio

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“…Additional evidence supporting an important role for fibrin(ogen) and clot formation in AD are the positive results obtained with anticoagulant therapy for this disease (Ratner et al, 1972; Walsh et al, 1978). Although those studies were small, the anticoagulant treatment either stopped the deterioration or provoked an improvement of the disease (Walsh, 1996).…”

Section: Discussionmentioning

confidence: 89%

Fibrinogen and β-Amyloid Association Alters Thrombosis and Fibrinolysis: A Possible Contributing Factor to Alzheimer's Disease

Cortes‐Canteli

Paul

Norris

et al. 2010

Neuron

296

416

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Summary Alzheimer's disease (AD) is a neurodegenerative disorder in which vascular pathology plays an important role. Since the β-amyloid peptide (Aβ) is a critical factor in this disease, we examined its relationship to fibrin clot formation in AD. In vitro and in vivo experiments showed that fibrin clots formed in the presence of Aβ are structurally abnormal and resistant to degradation. Fibrin(ogen) was observed in blood vessels positive for amyloid in mouse and human AD samples, and intravital brain imaging of clot formation and dissolution revealed abnormal thrombosis and fibrinolysis in AD mice. Moreover, depletion of fibrinogen lessened cerebral amyloid angiopathy pathology and reduced cognitive impairment in AD mice. These experiments suggest that one important contribution of Aβ to AD is via its effects on fibrin clots, implicating fibrin(ogen) as a potential critical factor in this disease.

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“…In human studies, placebo-treated dementia patients showed a significant deterioration in cognition, while warfarin-treated patients did not show any change in cognitive decline [46]. In addition, unregulated studies carried out several decades ago showed that the majority of dementia patients treated with warfarin presented with improved cognition compared to untreated patients [47, 48]. Furthermore, an epidemiological study on atrial fibrillation patients showed that long-term warfarin treatment is protective against dementia [49].…”

Section: Thrombotic/fibrinolytic System In Admentioning

confidence: 99%

Fibrinogen and Altered Hemostasis in Alzheimer's Disease

Cortes‐Canteli

Zamolodchikov

Ahn

et al. 2012

JAD

151

142

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Alzheimer’s disease (AD) is characterized by amyloid-β (Aβ) plaques, tau tangles, brain atrophy, and vascular pathology. Vascular defects include cerebrovascular dysfunction, decreased cerebral blood flow, and blood brain barrier (BBB) disruption, among others. Here, we review the evidence that links Aβ with the vascular pathology present in AD, with a specific focus on the hemostatic system and the clotting protein fibrinogen. Fibrinogen is normally found circulating in blood, but in AD it deposits with Aβ in the brain parenchyma and cerebral blood vessels. We found that Aβ and fibrin(ogen) interact, and their binding leads to increased fibrinogen aggregation, Aβ fibrillization, and the formation of degradation-resistant fibrin clots. Decreasing fibrinogen levels not only lessens cerebral amyloid angiopathy (CAA) and BBB permeability, but it also reduces microglial activation and improves cognitive performance in AD mouse models. Moreover, a prothrombotic state in AD is evidenced by increased clot formation, decreased fibrinolysis, and elevated levels of coagulation factors and activated platelets. Abnormal deposition and persistence of fibrin(ogen) in AD may result from Aβ-fibrin(ogen) binding and altered hemostasis and could thus contribute to Aβ deposition, decreased cerebral blood flow, exacerbated neuroinflammation, and eventual neurodegeneration. Blocking the interaction between fibrin(ogen) and Aβ may be a promising therapeutic target for AD.

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Senile‐Presenile Dementia: Follow‐Up Data on an Effective Psychotherapy‐Anticoagulant Regimen*

Cited by 54 publications

References 5 publications

The blood clotting Factor XIIIa forms unique complexes with amyloid‐beta (Aβ) and colocalizes with deposited Aβ in cerebral amyloid angiopathy

The blood clotting Factor XIIIa forms unique complexes with amyloid‐beta (Aβ) and colocalizes with deposited Aβ in cerebral amyloid angiopathy

Fibrinogen and β-Amyloid Association Alters Thrombosis and Fibrinolysis: A Possible Contributing Factor to Alzheimer's Disease

Fibrinogen and Altered Hemostasis in Alzheimer's Disease

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