Lecture 1 – Introduction: Breaking Alzheimer’s

Throughout most of human history, senile dementia (which occurs after age 65) has been considered a natural part of the aging process. It was not until the 20th century that scientists began to investigate and hypothesize regarding the cause of senile dementia more seriously. At the turn of the century, Dr. Alois Alzheimer was the first to discover and associate certain neuropathology with dementia. Specifically, he observed the accumulation of amyloid plaques between neurons and the presence of neurofibrillary tangles within neurons.  

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Importantly, Alzheimer’s disease was first recognized as a rare type of presenile dementia but not a cause of senile dementia. Most researchers believed that hardening of the arteries (atherosclerosis) was the primary cause. It was not until the 1960s that senile dementia began to be classified into subtypes. In the 1960s, it became clear that many older persons with the classical representation of senile dementia had neuropathology indistinguishable from Alzheimer’s disease when examined post-mortem. This condition was then called senile dementia of the Alzheimer’s type. Today, most cases of senile dementia are classified as either Alzheimer’s, vascular, Lewy body, or frontotemporal lobe dementia. Most dementia cases consist of mixed pathologies, not one or the other. Some have hardly any neuropathology, which means that assigning the causation of dementia to a particular neuropathology is illogical right from the beginning.  

Understanding the role of neuropathology in the etiology of dementia has been hindered by the obfuscation of certain words and definitions. The terms “Alzheimer’s pathology”, “Alzheimer’s disease”, and “dementia of the Alzheimer’s type or Alzheimer’s dementia” are often used interchangeably. This is made worse because Alzheimer’s disease and Alzheimer’s dementia are abbreviated as “AD”. These three “Alzheimer’s” terms have three different meanings. 

“Alzheimer’s pathology” is the purest of these terms and refers to the direct measurement of amyloid plaque or neurofibrillary tangle density in a brain region. It is not an interpreted value – it is what it is. 

“Alzheimer’s disease” is the neuropathological classification of a person as determined by a neuropathologist. Following an autopsy, a neuropathologist will review the neuropathological data across multiple brain regions and using one of several different neuropathological scaling systems make a collective determination of the severity of Alzheimer’s pathology – none, low, moderate, severe. This is purely neuropathological – there is no consideration made as to the clinical state of the person prior to death. 

“Alzheimer’s dementia” is the combination of two separate clinical determinations. First, there must be a determination of dementia. Dementia is not a pure measurement either, it is a clinical classification. A doctor will review a variety of cognitive test results and in some cases caregiver interview data using various cognitive scaling systems and make a collective determination of the severity of cognitive impairment – none, mild, moderate, severe. A person who has reached a threshold of cognitive impairment sufficient to warrant a diagnosis of dementia and who has reached a threshold of Alzheimer’s pathology sufficient to warrant a diagnosis of Alzheimer’s disease is classified as having dementia of the Alzheimer’s type, or Alzheimer’s dementia. 

Accordingly, Alzheimer’s pathology and cognition are separate objectively measured “facts” which can later be used to create a clinical classification. Any relationship that scientists intimate exists between two or more facts is not a fact but a hypothesis. The coexistence of facts is real and valid and does not need to be questioned unless there is fraud, which is not being suggested. The use of the term “dementia of the Alzheimer’s type” is a factually accurate and objectively determinable observation. It is simply the classification of a person. And it is no different than classifying a car as “blue with bald tires”. We are just stringing objective facts together. No reasonable person would assume that the color blue has anything to do with the baldness of tires. Likewise, there is no reason to assume that Alzheimer’s has anything to do with dementia simply because they coexist and are written together in a sentence.  

I created Breaking Alzheimer’s: The Definitive Lecture Series as a detailed scientific treatise to continue the awakening process that I began in Breaking Alzheimer’s – The Book. The Definitive Lecture Series is designed such that interested lay persons and scientists can obtain a full and complete understanding of the key aspects of brain health changes that are associated with Alzheimer’s disease and cognition. The series is organized into the following lectures: 

Lecture 1 – Introduction 

Lecture 2 – Philosophical Underpinnings 

Lecture 3 – Biochemistry of Cognition 

Lecture 4 – Biochemistry of Brain Volume 

Lecture 5 – Biochemistry of Neurofibrillary Tangles 

Lecture 6 – Biochemistry of Amyloid 

Lecture 7 – Biochemistry of APOE 

Lecture 8 – Plasmalogens and the Epidemiology of Dementia 

Lecture 9 – Biochemistry of Oxidative Stress 

Lecture 10 – Biochemistry and Clinical Efficacy of Plasmalogen Precursors 

In each lecture, Dr. Goodenowe explains the relevant research and literature of each topic. The lectures integrate Dr. Goodenowe’s own research and over 50 years of research from leading researchers from around the world.