Skip to main content
Brainlift-Program_Atrophic-Alzheimers.png

8 Signs of Atrophic Alzheimer’s Disease

Low nutrients and hormones

Micronutrient and hormone levels are suboptimal…your brain is starving.

Slower Onset

Slower progression (about 10 years) and later-onset than other AD subtypes.

Abnormal Insulin

Insulin levels are either too high (insulin resistance) or too low (not enough growth factor).

No Inflammation

Labs show low inflammatory markers (which is the opposite of other subtypes).

Poor Short Term Memory

Difficulty learning new things and storing new memories and information.

Better Long Term Memory

No problems recalling memories from when you were younger.

Brain Volume Loss

Measurable loss in the hippocampus region of the brain and brain synapses dried up.

ApoE Genetic Risk

One copy of ApoE4 gives you a 30% chance of getting AD. Two copies give you a 50% chance.

Subtype No. 2

Atrophic

Alzheimer’s Disease

The atrophic Alzheimer’s subtype is associated with a “failure to thrive” brain.

Your brain is made up of several different cell types. Most people are familiar with nerve cells (i.e. neurons), which conduct electrical signals via specific pathways that make possible everything you do each day, including thinking, breathing, swallowing, moving, sleeping, etc.

In order to support cell growth in the brain, your body has to produce the necessary growth factors. This has been a rapidly expanding area of research, and the results have been game-changers in the realm of understanding and treating neurodegenerative conditions like Alzheimer’s disease (AD).

GROWTH FACTOR

Brain Derived

Neurotrophic Factor

The most important growth factor is called brain derived neurotrophic factor (BDNF). If you can increase BDNF, with the right supportive environment, you can stimulate the growth of new neurons, and support the health and connecting networks of existing neurons, even into your old age.

BRAIN SUPPORT

Healthy Cell

Growth & Longevity

Other important factors that support healthy cell growth and longevity in the brain include optimized hormone levels (adequate thyroid and sex hormones, avoiding excessive stress hormones), optimized micronutrient levels, and frequent cognitive stimulation and learning.

Rapid withdrawal of support can be the most damaging, such as can happen with the removal of a woman’s ovaries as part of a complete hysterectomy.

“Imagine a barren landscape devoid of the support required to sustain life. This is the atrophic Alzheimer’s brain—shrinking and starved of nutrients, hormones, and everything else the brain needs to flourish. It’s critical to take steps now to promote a robust and sustainable growth environment for your brain.”

Dr. Scott Noorda, DO

Family Physician, Precision Medicine

Signs + Symptoms

of ATROPHIC ALZHEIMER’S DISEASE

The atrophic subtype of Alzheimer’s, like the inflammatory subtype, most often begins with the loss of ability to store new information and new memories, and also a harder time learning new things. Interestingly, long term memory is not lost, especially in the earlier stages of the disease process.

This means that people can recall sometimes minute details of events that happened 30, 40, or even 50 years ago, but may not be able to remember their conversation from five minutes ago. They also, like people suffering from the inflammatory subtype, initially retain their ability to speak, perform mathematical calculations, spell, and write.

The symptoms not only result from atrophy (shrinkage) of the memory centers of the brain (especially the hippocampus), but also because support for brain synapses (where one nerve connects to another) has dried up. This means that the ability to pass along signals from one area of the brain to another, or from the brain to different parts of the body, is compromised.

This process develops slowly, and often the symptoms aren’t recognized by the patient, so he/she will frequently protest that nothing is wrong.

Genetic Factors

of ATROPHIC ALZHEIMER’S DISEASE

Some subtypes of Alzheimer’s are more commonly associated with specific genetic susceptibilities. This is true for the atrophic subtype, which is more commonly associated with the higher risk ApoE4 gene, whether homozygous (two copies) or heterozygous (single copy).

When compared with the inflammatory subtype, people suffering from an atrophic subtype of AD typically develop symptoms at an older age, often 10 years later in life. (1)

Lab Indications

of ATROPHIC ALZHEIMER’S DISEASE

Different subtypes can’t always easily be distinguished by lab testing, but there are some unique findings in the atrophic subtype that are worth mentioning.

First, there are typically no markers of inflammation seen on the blood work. In fact, interestingly, inflammatory markers may even be lower than normal.

Second, suboptimal levels of multiple different types of hormones are frequently seen. These can include thyroid hormones, adrenal (or stress) hormones, sex hormones (such as estrogen, progesterone, and testosterone), and pregnenolone (the precursor hormone from which all other hormones are made).

Low levels of several different micronutrients can also be seen in this subtype of AD, including low vitamin D and low B-vitamins, specifically B12 and/or folate (vitamin B9). It’s important that your doctor test you not only for the amounts of B12 & folate in your blood but also that you are tested for homocysteine, which helps us know if you are converting those B-vitamins to their active (or methylated) form and utilizing them effectively.

Another possible finding in the atrophic subtype of AD is an abnormal insulin level, either too high (showing underlying insulin resistance) or too low. Insulin is needed as a growth factor for the brain, but too much of it, caused by unhealthy levels of glucose in the blood, can also be detrimental.

Target levels for these nutrients and hormones aren’t always the levels shown as normal by different lab companies. Discuss them with a practitioner trained in optimizing and personalizing these lab findings.

Schedule a Personalized Lab Consultation
REFERENCES
1.  Vaynman, S., Ying, Z., & Gómez‐Pinilla, F. (2004). Exercise induces BDNF and synapsin I to specific hippocampal subfields. Journal of neuroscience research, 76(3), 356-362.2. Reyes-Izquierdo, T., Nemzer, B., Shu, C., Huynh, L., Argumedo, R., Keller, R., & Pietrzkowski, Z. (2013). Modulatory effect of coffee fruit extract on plasma levels of brain-derived neurotrophic factor in healthy subjects. British Journal of Nutrition, 110(3), 420-425.
2.  Zhang, L., Fang, Y., Xu, Y., Lian, Y., Xie, N., Wu, T., … & Wang, Z. (2015). Curcumin improves amyloid β-peptide (1-42) induced spatial memory deficits through BDNF-ERK signaling pathway. PloS one, 10(6), e0131525.
3.  Ortiz-López, L., Márquez-Valadez, B., Gómez-Sánchez, A., Silva-Lucero, M. D. C., Torres-Pérez, M., Téllez-Ballesteros, R. I., … & Ramírez-Rodríguez, G. B. (2016). Green tea compound epigallo-catechin-3-gallate (EGCG) increases neuronal survival in adult hippocampal neurogenesis in vivo and in vitro. Neuroscience, 322, 208-220.
4.  Hadjighassem, M., Kamalidehghan, B., Shekarriz, N., Baseerat, A., Molavi, N., Mehrpour, M., … & Meng, G. Y. (2015). Oral consumption of α-linolenic acid increases serum BDNF levels in healthy adult humans. Nutrition journal, 14(1), 20.
5.  Rao, J. S., Ertley, R. N., Lee, H. J., DeMar Jr, J. C., Arnold, J. T., Rapoport, S. I., & Bazinet, R. P. (2007). n-3 polyunsaturated fatty acid deprivation in rats decreases frontal cortex BDNF via a p38 MAPK-dependent mechanism. Molecular psychiatry, 12(1), 36-46.
6.  Romo-Araiza, A., Gutiérrez-Salmeán, G., Galván, E. J., Hernández-Frausto, M., Herrera-López, G., Romo-Parra, H., … & Ibarra, A. (2018). Probiotics and prebiotics as a therapeutic strategy to improve memory in a model of middle-aged rats. Frontiers in Aging Neuroscience, 10, 416.
7.  Cahn, B. R., Goodman, M. S., Peterson, C. T., Maturi, R., & Mills, P. J. (2017). Yoga, meditation and mind-body health: increased BDNF, cortisol awakening response, and altered inflammatory marker expression after a 3-month yoga and meditation retreat. Frontiers in human neuroscience, 11, 315.
8.  Nikoletopoulou, V., Sidiropoulou, K., Kallergi, E., Dalezios, Y., & Tavernarakis, N. (2017). Modulation of autophagy by BDNF underlies synaptic plasticity. Cell metabolism, 26(1), 230-242.
9.  Khairy, E. Y., & Attia, M. M. (2019). Protective effects of vitamin D on neurophysiologic alterations in brain aging: role of brain-derived neurotrophic factor (BDNF). Nutritional neuroscience, 1-10.
10.  Hsiao, Y. H., Hung, H. C., Chen, S. H., & Gean, P. W. (2014). Social interaction rescues memory deficit in an animal model of Alzheimer’s disease by increasing BDNF-dependent hippocampal neurogenesis. Journal of Neuroscience, 34(49), 16207-16219.
11.  Molteni, R., Barnard, R. J., Ying, Z., Roberts, C. K., & Gómez-Pinilla, F. (2002). A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning. Neuroscience, 112(4), 803-814.
12.  Bredesen, D. (2017). The End of Alzheimer’s: The first program to prevent and reverse cognitive decline. Penguin. pp. 126-132.