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.;
Importantly, Alzheimer’s disease was first recognized as a rare type of pre-senile 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.
Breaking Alzheimer's
Breaking Alzheimer's is Dr. Dayan Goodenowe’s story of personal and scientific perseverance. The biochemical mechanisms of neurological disease is his area of expertise and was his area of expertise for 15 years before he serendipitously discovered that low plasmalogen levels were causing Alzheimer’s.
Dr. Goodenowe had never heard of plasmalogens and he had never been taught about them. There are now 15 years of supportive validation of this discovery and access to plasmalogen testing and supplementation is now available to everyone. By sheer will, Dr. Goodenowe has completed the beginning and the middle of this journey such that the plasmalogen genie cannot be put back in the bottle. This book is about bringing the reader up to speed as to where we currently are on this journey and where we are going from here.
Dr. Goodenowe Breaking Alzheimer’s: The Definitive Lecture Series
Created as a detailed scientific treatise to continue the awakening process that he began in Breaking Alzheimer’s – The Book. The Definitive Lecture Series is designed to obtain a full and complete understanding of the key aspects of brain health changes that are associated with Alzheimer’s disease and cognition.
In each lecture, Dr. Goodenowe explains the relevant research and literature on each topic. The lectures integrate Dr. Goodenowe’s own research and over 50 years of research from leading researchers from around the world.
Breaking RCDP
Dr. Goodenowe found out about the rare disease Rhizomelic Chondrodysplasia Punctata (RCDP) through his work in Alzheimer’s disease, where he discovered that plasmalogen deficiency causes Alzheimer’s disease. RCDP affects approximately 1 in 100,000 children.
The disease has a very precisely defined biochemical cause – children are unable to make precursors for plasmalogens. Affected children quickly become severely plasmalogen deficient. Because adequate plasmalogen levels are essential for numerous biological functions such as myelination, neurological function, neuromuscular function, cholesterol regulation, lung function, cardiac function, vision, neurogenesis and more, these children suffer severe direct and indirect health consequences.
Dr. Goodenowe has prepared the Definitive Lecture Series on RCDP to break down the disease so that anyone interested can learn about the biochemical disease process, how it leads to functional impairments, and what we can do to work with the biochemistry to improve function.
CLINICAL RESEARCH
Diseases don’t cause dysfunction; dysfunction causes disease. Decades of clinical research have taught Dr. Goodenowe that diseases are an opportunity to learn more about optimal health.
- Restore function. Cure disease.
- Maintain function. Prevent disease.
- Optimize function. Achieve vitality.