CovidHelp Resources - Level 1

Information You Can Use!

It’s not always easy to know where to go to find what you’re looking for, and sometimes one does not know what one is looking for until one has found it.

Here we will list a variety of websites, videos, and podcasts for your research pleasure. Some of these sites are fairly simple and easy to navigate, while others offer so much information, it’s downright overwhelming.

We have broken it down a bit in an attempt to keep everyone properly “whelmed”. Don’t feel bad if the more you learn, the more you realize you don’t know.

Life is a Journey and learning is part of the adventure. Enjoy!

Breaking Alzheimer's

Dr. Dayan Goodenowe, PhD

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.

Dr. Goodenowe created Breaking Alzheimer’s: The Definitive Lecture Series 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.  

Image

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.

Image

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.

More links

Print