AD & IPF--Its All About Clotting

Alzheimer’s disease AD and Idiopathic Pulmonary Fibrosis IPF

Tau is finally considered the culprit, after pursuit of beta-amyloid control for decades. Tau is the tough to dissolve tangle compared with beta-amyloid deposition; fibrinogen is strongly implicated in the development of tau tangles. Cerebral-vascular events and myocardial events are well-known to be the result of plaque formation, thrombi and DIC, among other clotting disorders.

Apparently, dementia, idiopathic pulmonary fibrosis and Alzheimer's Disease #Alzheimers are among the various clinical manifestations of clotting disorders. Paroxysmal strokes occur when clots pass through a patent foramen ovale. On a microscopic scale, tau tangles develop as thick proteinaceous materials flow freely from the right to left atrium and onto the cerebral circulation.

Objective physical findings / measurements which will predict and guide treatment options years’ ahead of cognitive disorder onset:

• Serum fibrinogen and clotting factor measurements to test for hypercoagulability

• Cardiac ultrasound / MRI / angiocatheterization / phonocardiography to determine the presence and extent of patent foramen ovale in a given individual.

Persons afflicted with Down Syndrome (trisomy 21) in general have a patent foramen ovale, increased levels of fibrinogen and other clotting proteins, and virtually 100% do develop signs and symptoms of AD by age 65.

Persons with patent foramen ovale without trisomy 21 have a significant increase in incidence and prevalence of AD.

Persons without a patent foramen ovale but with increased fibrinogen and clotting proteins develop idiopathic pulmonary fibrosis IPF.

Persons with a patent foramen ovale have paradoxical strokes from blood clots traveling to the heart in the venous return entering the heart, bypassing the filtration of the lungs, traveling through the patent foramen ovale and pumped to the brain by the left ventricle.

The keys to determining who is probably going to develop AD are determining the presence of PFO (patent foramen ovale) and/or increased fibrinogen and clotting protein levels. A PFO and increased clotting proteins is the worst combination and will result in end-organ events including cerebral vascular accidents, myocardial infarctions, thrombosed kidneys, pancreas and other vital structures.

The key to determining who is probable to develop IPF is very probably a finding of increased fibrinogen and clotting protein levels, along with various genetic predispositions to pulmonary disease.

Hypercoagulable blood passing through a PFO without filtering and biochemical changes in the lungs will coat the neurons with a continuous and thick fluid layer of proteins, essentially coating neurons nearest the brain capillaries with proteinaceous plaques (Tau tangles and beta amyloid plaques). Tau tangles have a high concentration of fibrinogen and are difficult to dissolve. Coated neurons are dead neurons.

The key to treatment of AD (and IPF) is accurate prediction of measureable objective findings necessary for the eventual development of disease and intervening sufficiently early, even decades ahead, with new drugs designed to keep fibrinogen and other clotting proteins at acceptable, function and not at hypercoagulable levels. Cessation of smoking is of paramount importance in prevention of all vascular disease.

AD and IPF are associated with smoking cigarettes. Fibrinogen dramatically increases with cigarette smoking. Fibrinogen increases linearly with age resulting in hypercoagulable states in all persons eventually. Fibrinogen and hypercoagulable conditions promote coronary artery disease CAD and strokes.

The evidence is mounting and the fog is clearing. Perhaps you should focus your efforts on understanding clotting proteins, platelet function/dysfunction, DIC...beta-amyloid deposition apparently is not the culprit.