Types of Alzheimer's Disease

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Jul 12, 2024

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Types of Alzheimer's Disease 

Different researchers classify Alzheimer's Disease using vastly different stages.  Alzheimer's Disease has a genetic component that becomes active in some people and dormant in others. Alzheimer’s creates an environment that promotes brain changes in those affected.  Lastly, amyloid plaque is the brain’s protective response to vastly different lifestyle insults.

Alzheimer’s Disease is an imbalance of multiple systems within the body. 

People with Alzheimer’s disease usually have more than one type and present multiple risk factors.

One of the things I like most about breaking Alzheimer’s into types is once you know where you stand, it is easy to begin to resolve. Dr. Bredesen’s books provide many examples from his patients.  

 Also, please keep in mind that in the descriptions below, I am cutting and pasting most of the information.  I do not want to risk misinterpreting any of Dr. Bredesen’s research and misinforming you. 

Type 1

Type 1’s primary characteristic is inflammation.  It tends to run in families as it is common in people who carry one or two ApoE4 alleles (ApoE in itself is considered an inflammatory gene). Individuals begin to lose the ability to store new information in the hippocampus – for individuals who carry two copies of ApoE4 this tends to start in the late fifties or early sixties. For those with no copies of ApoE4, symptoms present typically in the sixties or seventies. A reduced hippocampal volume – chronic inflammation encourages the brain to destroy synapses faster than it creates them.


Biochemical Markers of Type 1

  • An increase in C-reactive protein (CRP), which is made by the liver in response to inflammation.
  • A decrease in the ratio of albumin to globulin.
  • An increase in interleukin-6.
  • An increase in tumor necrosis factor.
  • Additional metabolic and hormonal abnormalities such as insulin resistance

 Type 2

Type 2’s primary characteristic is low levels of nutrients, hormone factors, and/or trophic factors.  Type 2 also occurs more frequently in those who carry one or two copies of the ApoE4 allele, but the symptoms tend to initiate about a decade later than the inflammatory Type 1. Individuals begin to lose the ability to form new memories in the hippocampus. However, there is little to no evidence of inflammation – sometimes inflammatory markers may be lower than normal.

Biochemical Markers of Type 2

Levels of hormones such as thyroid, adrenal, estrogen, progesterone, testosterone, and pregnenolone tend to be suboptimal. The optimal hormone ranges are:

  • TSH: less than 2.0 mIU/L
  • Free T3: 3.2-4.2 pg/mL
  • Free T4: 1.3-1.8 ng/dL
  • Reverse T3: less than 20 ng/dL
  • AM Cortisol: 10-18 mcg/dL
  • Pregnenolone: 100-250 ng/dL
  • Estradiol: 50– 250 pg/ mL (women, age-dependent)
  • Progesterone: 1-20 ng/mL (women, age-dependent)
  • Testosterone: 500-1,000 ng/dL (men) 25-70 ng/dL (women)

A decrease in serum Vitamin D levels. Normal Vitamin D levels should be 50-80 ng/mL.

An increase in homocysteine levels can occur. Normal homocysteine levels should be less than or equal to 7 μmol/ L (homocysteine is also seen to increase in Type 1)

Insulin resistance can occur OR insulin levels may be too low.

Type 1.5

Type 1.5’s primary characteristic is insulin resistance (diabetes). Type 1 and Type 2 Alzheimer’s Disease can occur together – often seen with neural inflammation in addition to the reduced support for brain synapses. A commonly seen combination of type 1 and type 2 AD is known as Type 1.5 or glycotoxic Alzheimer’s Disease.

Biochemical Markers of Type 1.5

Although characteristics are similar to those found in Type 1 and Type 2 AD, blood glucose levels and hemoglobin A1c are chronically high in Type 1.5 which results in inflammation.

  • Normal fasting blood glucose levels should be between 70-90 mg/dL
  • Normal hemoglobin A1c levels should be 4.0-5.3%

High levels of insulin that are secreted in response to this high blood glucose level lead to insulin resistance. This results in a loss of trophic support. Trophic support refers to a variety of chemical signals that neurons need to continue living. Brain cells die and the brain shrinks when you experience a loss of trophic support.

Neurons are energetically expensive cells. They use a lot of oxygen and require a large expenditure of energy in the form of ATP to do their normal functions. As part of homeostatic adjustment, the body prefers to minimize extra energy usage. However, since neurons are critically important for healthy functioning, they receive signals in the form of chemicals that tell them to continue working. These chemicals are called trophic factors.

Many of these trophic factors are synthesized and released by glial cells of the nervous system, the non-neuronal cells that interact closely with the neurons. Glial cells, particularly the astrocytes and Schwann cells, are well-known producers of trophic support molecules.

One of the best-characterized trophic support molecules is called brain-derived neurotrophic factor, or BDNF. BDNF is a large protein. BDNF is normally synthesized and produced by cells of the nervous system and is important for making changes in neurons or for the growth of nerve cells. BDNF signals through the activity of several different receptors, the most well-known being the TrkB receptor. 

Other neurotrophic factors used by the nervous system that are important as trophic support molecules include nerve growth factor (NGF), neurotrophin-3, glial-derived neurotrophic factor (GDNF), and ephrins. Trophic factors, such as NGF and BDNF, control the development and survival of specific groups of neurons.

 Type 1, Type 1.5 & Type 2 Alzheimer’s Disease lead to the imbalance between the production and destruction of neural synapses.

 Type 3

Type 3’s primary characteristic is exposure to toxins such as mercury, toluene, benzene (candles), or mycotoxins (mold). Type 3 tends to occur in those who have the ApoE3 allele rather than ApoE4 and does not typically run in families.

Type 3 hits individuals at younger ages, typically late forties to early sixties. Symptoms do not begin with memory loss but rather with cognitive difficulties involving numbers, speech, or organization. Individuals will start seeing difficulties with:

  • Math, such as calculating tips or bills.
  • Speech, such as finding the right words, or spelling or reading correctly.
  • Rules of games, such as poker or bridge.
  • Depression and attention deficits are common.

The brain ultimately loses recent and old memories.

Patients with Type 3 are often diagnosed initially with something other than Alzheimer’s Disease such as depression or frontotemporal dementia.

 Biochemical Markers of Type 3

  • Low triglyceride levels as compared to cholesterol levels.
  • MRI scans show shrinkage of the hippocampus.
  • Neuroinflammation and vascular leaks are presented on a specific MRI called FLAIR (Fluid-attenuated inversion recovery) as white spots.
  • Decreased zinc levels. Normal levels are between 90-110 mcg/dL.
  • Elevated copper levels. Normal copper levels are between 90-110 mcg/dL.
  • High blood levels of toxic chemicals such as mercury or mycotoxins (caused by molds).
  • The pituitary gland and adrenal glands become dysfunctional, which can show up in lab tests as hormonal abnormalities.

Type 4

Type 4’s primary characteristic is low blood flow to the brain. Type 4 or Vascular Alzheimer’s Disease, is caused by a reduction of blood flow to the brain, which ultimately deprives the brain of essential oxygen and nutrients. The brain is an extremely vascularized tissue, meaning it requires large amounts of oxygen. A lack of oxygen to the brain leads to hypoperfusion (low blood flow) and compromises the blood-brain barrier which allows for harmful substances to leak in and damage neurons. Cerebral vasculature is extremely important as it is one way the body clears the accumulation of amyloid-beta.

Biochemical Markers of Type 4

“Leakiness” present in vascular tissues.

Individuals with cardiovascular disease have a high risk for Type 4 Alzheimer’s.

These individuals do best when they prioritize healing underlying insulin resistance.

 Type 5

Type 5’s primary characteristic is brain damage. Type 5 or trauma-induced Alzheimer’s, results from traumatic brain injuries (TBI) which disrupt normal brain function, including learning and thinking skills. Certain types of TBI’s may increase the risk of developing Alzheimer’s disease years after the injury takes place.

One of the most impactful studies showed that those with a history of moderate TBI had a 2.3 times greater risk of developing Alzheimer’s than older adults with no history of a head injury and those with a history of severe TBI had a 4.5 times greater risk.

Biochemical Markers of Type 5

There are no biochemical markers for Type 5 as it is triggered by injuries to the brain such as:

  • Blunt force trauma
  • Concussions
  • Physical Abuse
  • Chronic traumatic encephalopathy (CTE)

Now that we have broken down Alzheimer’s Disease into 6 different types and identified their characteristics and potential causes we can begin to address what you need to do to prevent and begin to heal the damaging insults to the brain.  We will begin to work on that next week. 

OR if you want to jump ahead, purchase Dr. Dale Bredesen’s books.  Here are the links to purchase them on Amazon.

The End of Alzheimer’s 2 Books Collection Set By Dale Bredesen Paperback – October 26, 2023

LINK: https://amzn.to/462LcY3 

The End of Alzheimer's Program: The First Protocol to Enhance Cognition and Reverse Decline at Any Age Paperback – September 6, 2022

LINK: https://amzn.to/3xNcrct

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