Nootropics and Aging

Do you want to live longer? Forever even? Some people may answer “yes” while others may answer “no”. Regardless of your answer, what would be the point in prolonging your life if you had to live in a state of confusion and dementia? It’s a fact that Alzheimer’s disease affects 1 in 10 people over the age of 65 and almost half of people over the age of 85.[1]Keep in mind that there are many other cognitive disorders associated with age including delirium, dementia, and amnesia.

Unless you do something to mitigate your chances of contracting a cognitive disorder, more likely than not, you will end up suffering from one. As painful as it is to think about, this means your last living years will be spent in a state of confusion, suffering, and panic. People who suffer from Alzheimer’s experience severe loss of memory, disorientation with respect to time and place, lose their ability to reason and experience irrational mood swings. [1] A fate some people would categorize as being worse than death.

Now the important question is, “Can I extend my life while at the same time lowering my chances of succumbing to a cognitive disorder?” The short answer is “Yes”. In order to understand why the answer is “Yes”, you first must understand what is going on in your brain while you age, and what can cause a cognitive disorder such as Alzheimer’s.

Structural Changes

As we age our brain accumulates structural damages. These damages can be contributed to “Oxidative Stress” caused by Free Radicals. A free radical is an atom, molecule, or ion with unpaired electrons.  Having unpaired electrons cause these atoms to be extremely chemically reactive. When these free radicals are allowed to run free throughout the body they cause damage to cells all over the body. What’s worse is that cells in the brain are abnormally sensitive to these free radicals. [2] Not only does the damage caused by these free radicals contribute to cognitive degeneration but it is also linked to many types of cancer. [3]

Aging Research:

Science Direct: Neurobiology of Aging

An in-depth and scientific explanation on the subject of cognitive aging

The primary site of free radical damage is mitochondrial DNA (mtDNA). [2] The mtDNA contained in each cell provides chemical instructions required for the cell to function. As damage to mtDNA builds up the cells lose their ability to function. This results in a number of negative consequences in your brain:

Your Brain is losing its Plasticity [4]

Plasticity refers to your brains ability to form, strengthen, weaken, and destroy neuronal connections. The more plastic your brain is, the better your brain can effectively communicate with itself. Your ability to form and store memories is closely tied to how synaptic your brain is. Synaptic plasticity is also closely tied with learning.

Dendrites levels and density in your brain decrease [5]

Dendrites are what conduct the chemical messages being sent through synaptic pathways. In other words, your brain cannot receive communications without them. Dendrite levels are also believed to play an important role in memory and learning.

Preventing Free Radical Damage

Regretfully, the production of these free radicals is completely normal. They are simply a byproduct produced when cells create energy. Production of free radicals can also be caused by exposure to radiation, pollution, and extreme levels of sunlight among other things. Even though it is not possible to lessen the production of free radicals due to natural cell functions it is possible to mitigate the damage they cause through Anti-Oxidants.

An anti-oxidant is simply a molecule that prevents the oxidation of other molecules. When a free radical attacks a molecule it steals an electron turning the molecule it attacked into a free radical. This chain reaction is what causes damage and eventually the death of cells in your body. Anti-oxidants stop this process from occurring which greatly reduces the damage cells take due to free radicals.

A number of nootropics and other supplements act as anti-oxidants. These nootropics include:

Chemical Changes

There is more than just structural changes taking place as you age. Your brain is also changing on a chemical level. Neurotransmitters are chemicals that neurons in your brain release to communicate with each other. As you age, levels certain neurotransmitters begin to change.

These chemical changes are caused by a decrease in gray matter which occurs as you age. [6] Gray matter is a vital component of the central nervous system.  It is made up of neurons that are involved in muscle control, memory, speech, emotions, and seeing. White matter is another component of the central nervous system. White matter allows messages to be passed from different areas of gray matter.

Think of your central nervous system as a network of computers. The gray matter represents the computers themselves. Without gray matter your brain could not calculate, problem solve, form speech, etc. The white matter represents the cables connecting the computers to each other. Without white matter, the computers in the network could not communicate with each other.

As the number of computers in your network decrease levels of neurotransmitters are affected. There are three neurotransmitters in particular that play an important role in the aging process.

Dopamine levels decrease

As you age you body is unable to synthesize dopamine as well and there is a significant decline in D1, D2, and D3 dopamine receptors. [7][8][9][10][11][12] Healthy levels of dopamine are critical for cognitive flexibility. Cognitive flexibility is your brain’s ability to switch its response to match your current situation. Without cognitive flexibility, your brain cannot perform executive functions. These functions include working memory, attention, problem solving, verbal reasoning, inhibition, multi-tasking, and planning. [13]

Dopamine levels begin to drop around the age of 45. Research shows that even the healthiest of humans die when dopamine levels in their brain drop below 30% of the standard level. [14]

Nootropics that elevate levels of dopamine:

  • Deprenyl – Multiple studies have shown that deprenyl helps elevate dopamine levels and extend one’s lifespan. Based on the research, in some cases it may extend one’s life by as much as 25%. It is also approved by the FDA to treat Parkinson’s Disease.

Serotonin levels decrease

Along with dopamine, serotonin synthesis and transportation declines. [12] Serotonin is very important for the regulation of mood, appetite, and sleep. It also plays a role in learning and memory.

Glutamate levels decrease

Studies have also shown a relationship between aging and glutamate levels. [15][16][17] There is also a relationship between neurological diseases and glutamate levels. [15] Glutamate plays a very important role in communication between neurons. [18]It is one of the several factors that contribute to your brains synaptic plasticity. This makes glutamate a vital part of memory and learning. [19]

Nootropics that sustain levels of glutamate:

  • Theanine – Acts as an precursor to glutamate

What Happens Differently to Cause Dementia?

Dementia, taken from the Latin word “madness” , refers to the serious loss of cognitive abilities in a previously unimpaired person.  This cognitive decline is characterized as being more severe than what you would normally expect from aging. Dementia is not a single disease, instead it refers to a broad range of illnesses which effect memory, problem solving, language, and attention. Dementia is caused by a wide variety of cognitive diseases. The most commonly known cause of dementia is Alzheimer’s disease. It accounts for between 50%-60% of dementia cases affecting those aged 65 or older. [20]

Preventing Alzheimer’s Disease

Currently the causes of Alzheimer’s disease are not well understand. There is currently no cure for this form of dementia. Treatments that are available only help with the symptoms of the disease. There is currently no drug that will stop or reverse the progression of Alzheimer’s. Even though the exact cause is not known, there are theories.

More Information:

Deprenyl, Dopamine, and Aging

Research shows that diminished levels of dopamine lead to death in the healthiest of people, Deprenyl may be the answer.

The hypothesis on which the majority of available drug treatments are based is the “Cholinergic Hypothesis” This hypothesis proposes that Alzheimer’s disease is caused by reduced levels of the neurotransmitter acetylcholine. A large number of therapeutic treatments have emerged that attempt to elevate acetylcholine levels and repair acetylcholine synthesis.  Some of these treatments have proven efficient in delaying the onset of Alzheimer’s symptoms. [20]

Interestingly, many of the nootropics listed on this site were originally developed to help treat and prevent the symptoms of Alzheimer’s and other causes of dementia. However, when used by perfectly healthy individuals they provide a boost to many of their cognitive functions.

Nootropics which effect the neurotransmitter acetylcholine and are designed to treat dementia include:

Which Nootropics Work Best?

When it comes to flat out extending your lifespan, Deprenyl is the most reliable. Countless studies have proven it’s effects are real. You don’t need to start taking it until you are 30 years old so for those of you who are still young just keep it in the back of your mind until later.

As for the anti-oxidants, green tea is the most studied and the most potent. It’s anti-oxidant properties exceed that of both vitamin C and vitamin E. It also provides a slew of other healthy benefits including a boosted immune system, decreased risk of cardiovascular disease, and a boost to metabolism. If you are looking to improve general health, green tea is an excellent option.

For preventing dementia, it’s hard to tell which works the best. If this is your goal, it is best to just work one or two of those nootropics into your regimen.

Keep in mind that these nootropics effect everyone differently. I encourage you to read all the material pertaining to each nootropic on this site and select one(s) that suit your specific set of needs.

Cited Sources

1. Welington Parc, Alzheimer’s Fact Sheer

2. Butterfield, A.; Ding, Q.; et al. (2005). “Evidence of increase oxidative damage in subjects with mild cognitive impairment”. Neurology 64 (7): 1152–1156. doi:10.1212/01.WNL.0000156156.13641.B.

3. Appleton, C.; Deary, I.; et al. (2004). “Cognitive reserve and the neurobiology of cognitive ageing”. Ageing Research Reviews 3 (4): 369-382. doi:10.1016/j.arr.2004.05.001.

4. Barnes, C.; Burke, S. (2006). “Neural plasticity in the ageing brain”. Nature Reviews Neuroscience 7 (1): 30-40. doi:10.1038/nrn1809.

5. Hof, P.; Morrison, J. (2004). “The aging brain: morphomolecular senescence of cortical circuits”. Trends in Neuroscience 27 (10): 607–613. doi:10.1016/j.tins.2004.07.013.

6. Henkenius, A.; Peterson, B.; et al. (2003). “Mapping cortical change across the human life span”. Nature Neuroscience 6 (3): 309–315. doi:10.1038/nn1008.

7. Hof, P. R.; Mobbs, C. V. (2009). Handbook of the neuroscience of aging. London: Elsevier. ISBN 9780123748980.

8. Kaasinen, V.; Vilkman, H.; Hietala, J.; Någren, K.; Helenius, H.; Olsson, H.; Farde, L.; Rinne, J. O. (2000). “Age-related dopamine D2/D3 receptor loss in extrastriatal regions of the human brain”. Neurobiology of Aging 21 (5): 683–688. doi:10.1016/S0197-4580(00)00149-4.

9. Wang, Y.; Chan, G. L. Y.; Holden, J. E.; Dobko, T.; Mak, E.; Schulzer, M.; Huser, J. M.; Snow, B. J. et al. (1998). “Age-Dependent Decline of Dopamine D1 Receptors in Human Brain: A PET Study”. Synapse 30 (1): 56-61. doi:10.1002/(SICI)1098-2396(199809)30:1<56::AID-SYN7>3.0.CO;2-J

10. Iyo, T.; Yamasaki (1993). “The detection of age-related decrease of dopamine, D1, D2 and serotonin 5-HT2 receptors in living human brain”. Prog. Neuro-Psycopharmacol & Biol. Psychait. 17: 415–421.

11. Rinne, Juha O.; Lonnberg, Pirkko; Marjamaiki, Paivi (1989). “Age-dependent decline in human brain dopamine D1 and D2 receptors”. Brain Research 508: 349–352. PMID 2407314.

12. Wong, D. F.; et al. (1984). “Effects of age on dopamine and serotonin receptors measured by positron tomography in the living human brain”. Science 266 (4681): 1393–1396. doi:10.1126/science.6334363.

13. Chan, R. C. K., Shum, D., Toulopoulou, T. & Chen, E. Y. H. (2008). “Assessment of executive functions: Review of instruments and identification of critical issues”. Archives of Clinical Neuropsychology. 2 23 (2): 201—216. doi:10.1016/j.acn.2007.08.010PMID 18096360


15. Chang, L.; Jiang, C. S.; Ernst, T. (2009). “Effects of age and sex on brain glutamate and other metabolites”. Magnetic Resonance Imaging 27 (1): 142–145. doi:10.1016/j.mri.2008.06.002.

16. Saliasuta, N.; Chang, L.; Ernst, T. (2008). “Regional variations and the effects of age and sex on brain glutamate and other metabolites”. Magnetic Resonance Imaging 26 (5): 667-675. doi:10.1016/j.mri.2007.06.007

17. Kaiser, L. G.; Schuff, N.; Cashdollar, N.; Weiner, M. W. (2005). “Age-related glutamate and glutamine concentration changes in normal human brain: 1H MR spectroscopy study at 4 T”. Neurobiology of aging 26 (5): 665-672. doi:10.1016/j.neurobiolaging.2004.07.001.

18. Cooke SF, Bliss TV (2006). “Plasticity in the human central nervous system”. Brain 129 (Pt 7): 1659–73. doi:10.1093/brain/awl082PMID 16672292.

19. Bliss TV, Collingridge GL (January 1993). “A synaptic model of memory: long-term potentiation in the hippocampus”. Nature 361 (6407): 31–39. doi:10.1038/361031a0PMID 8421494.

20. Francis PT, Palmer AM, Snape M, Wilcock GK (February 1999). “The cholinergic hypothesis of Alzheimer’s disease: a review of progress”. J. Neurol. Neurosurg. Psychiatr. 66 (2): 137–47. doi:10.1136/jnnp.66.2.137PMC 1736202PMID 10071091