Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Clement L. Trempe is active.

Publication


Featured researches published by Clement L. Trempe.


The End of Alzheimer's (Second edition)#R##N#The Brain and Beyond | 2017

Alzheimer’s Disease Prevention

Thomas J. Lewis; Clement L. Trempe

Alzheimer’s disease is preventable now that risk factors and causes are more well understood. Enhancement of immunity is a key factor in prevention. Also, fats that support overall brain health and reduce inflammation play a key role in prevention. The role of diet, exercise, internal homeostasis, gut health, and key micronutrients are explored.


Frontiers in Aging Neuroscience | 2018

It’s Never Too Early or Too Late—End the Epidemic of Alzheimer’s by Preventing or Reversing Causation From Pre-birth to Death

Clement L. Trempe; Thomas J. Lewis

The path to sporadic Alzheimer’s is a tragic journey beginning prior to birth and ending in the most dreaded disease of society. Along the disease path are a myriad of clues that portend AD, many of which are complaints of seemingly unrelated conditions from chronic migraines, mood disorders, eye diseases, metabolic syndromes, periodontal diseases, hormonal and autoimmune diseases. Properly treating, not just managing, these diseases, prior to onset of dementia, may significantly reduce dementia incidences. Current high levels of health complaints reflect a state of generalized poor health and compromised immunity. During the mid-Victorian era, people were long-lived yet healthy, suffering from chronic diseases at one tenth the rate of peoples today. It’s our poor health, at any age that increases susceptibility to chronic diseases and Alzheimer’s. Infection is involved in many cases of Alzheimer’s and other neurodegenerative diseases but is also implicated in many chronic conditions. Scientists looking for causation recognize that Alzheimer’ is multifactorial and systemic—not “brain only.” To slow, stop and reverse the AD epidemic, identification and reversal of causal factors must occur across the entire life spectrum of humans. This approach simply gives consideration to enhancing immune status of our bodies and brain, and controlling inflammation and infection, throughout the entire age spectrum. Infection is a causal factor, but the root cause is multi-factorial and immune health related. Pasteur stated it best when acknowledging the work of Bernard in 19th Century France, “The seed is nothing, the soil is everything.”


The End of Alzheimer's (Second edition)#R##N#The Brain and Beyond | 2017

Is it Alzheimer’s Disease?

Thomas J. Lewis; Clement L. Trempe

“Alzheimer’s” is an inadequate final diagnosis for this multifactorial condition. Hope is often restored when a broader and deeper diagnosis is performed. When such a medical diagnostic process is followed, treatable and often times reversible causes of Alzheimer’s are uncovered. Understanding true causes enables doctors to understand how to prevent the disease. And, when these causes are uncovered in a person with Alzheimer’s, there is a bona-fide possibility that their condition may be slowed, stopped, or even reversed.


The End of Alzheimer's (Second edition)#R##N#The Brain and Beyond | 2017

Differential Diagnosis Toward a Cure for Alzheimer’s

Thomas J. Lewis; Clement L. Trempe

To truly cure Alzheimer’s disease, patients must not accept a diagnosis that simply describes symptoms. They must demand that doctors dig deeper into causes and better define risks. This chapter walks through a proper process of diagnosis that then leads to healing treatment. It also clarifies Alzheimer’s risks and what an individual can do to ameliorate those risks. Finally, why there is hope for all Alzheimer’s sufferers today is explained.


The End of Alzheimer's (Second edition)#R##N#The Brain and Beyond | 2017

Diagnosis of Alzheimer’s—Standard-of-Care

Thomas J. Lewis; Clement L. Trempe

The standard and accepted diagnosis of Alzheimer’s and other dementias has proven inadequate at providing clinicians with any tools to modulate the disease. The main reason for the lack of progress in Alzheimer’s disease is the presumption that it is a brain only disease. The consensus group that developed and continues to develop standard-of-care diagnostic and treatment standards and advice is an assembly of brain-only scientists and doctors. They abjectly ignore the possibility that Alzheimer’s is a sick brain in a sick body. This chapter reviews the current standard diagnostic process and explains their shortcomings.


The End of Alzheimer's (Second edition)#R##N#The Brain and Beyond | 2017

Can Medicine Save You

Thomas J. Lewis; Clement L. Trempe

The commercialization of healthcare, that is, business usurping the authority and power of doctors in the healthcare delivery model, has created misalignment between health and profit. Doctors are now controlled by the payer system that causes them to see more patients in less time, or prescribe expensive procedures just to review the salary they were accustomed to when they were in control of health care. As a consequence, the time and energy to make a proper root-cause diagnosis has been replaced with an expedient symptoms-only diagnosis and prescriptions. This chapter explores many forces that have made medicine both unaffordable and ineffectual.


The End of Alzheimer's (Second edition)#R##N#The Brain and Beyond | 2017

The Amyloid Cascade Hypothesis

Thomas J. Lewis; Clement L. Trempe

The amyloid cascade hypothesis has been essentially the only theory and mechanism of Alzheimer’s disease pursued for drug development. Over the past three decades dozens of therapeutics that targeted the various stages of amyloid development—by various mechanisms—have failed to impact the course of the disease in patients involved in clinical trials. These results call into questions the involvement of amyloid in the genesis of Alzheimer’s. Amyloid provides some utility in detection of the disease, but is not a viable treatment target.


The End of Alzheimer's (Second edition)#R##N#The Brain and Beyond | 2017

A New Diagnostic Paradigm

Thomas J. Lewis; Clement L. Trempe

Our healthcare system reacts to chronic disease. A major reason is a lack of available predictive tests in use. These tests exist, are low cost, and are readily available, but are largely ignored. This chapter highlights the use of the eye in screening and early detection of diseases. The diseases that can be “caught” through an eye exam, long before a patient either has symptoms of disease or suffers an adverse event, include cardiovascular diseases and Alzheimer’s disease.


The End of Alzheimer's (Second edition)#R##N#The Brain and Beyond | 2017

Inflammation Friend or Foe

Thomas J. Lewis; Clement L. Trempe

Most experts agree that inflammation is involved in the Alzheimer’s cascade, however few if any clinicians test for inflammation because it is managed as a “brain only” disease in clinical practice. This chapter illustrates the strong association between systemic, whole body inflammation, and Alzheimer’s disease. Inflammation is a treasure and a proper diagnosis of Alzheimer’s must include a determination of the causes—then the treatments—of the inflammation. Ways to test for and treat inflammation are included.


The End of Alzheimer's (Second edition)#R##N#The Brain and Beyond | 2017

Does Infection Cause Alzheimer’s?

Thomas J. Lewis; Clement L. Trempe

Infection plays a major role in many cases of Alzheimer’s. Infection is not the root cause of Alzheimer’s but contributes to and exacerbates neuroinflammation in vulnerable hosts. Those with Alzheimer’s and infection may be able to realize significant improvement in their condition when the insulting infection is identified and properly treated. Spirochetes and other intracellular pathogens are the main infectious species tied to Alzheimer’s. However, viruses and multicellular pathogens are also implicated in the disease.

Collaboration


Dive into the Clement L. Trempe's collaboration.

Researchain Logo
Decentralizing Knowledge