Learning and memory – types of memory, memory loss, Amnesia, Alzheimer’s Disease – Innovita Research

Learning and memory – types of memory, memory loss, Amnesia, Alzheimer’s Disease

Learning new things is a natural process for everyone. We learn something new every day from an early age. Thanks to the possibility of learning new things, we can discover the reality around us and function well in it. Learning is the process of getting information from the surroundings.

Image credit: Pixabay (Free Pixabay license)

Memory refers to storing, processing, and recalling that information. Human memory has the ability to preserve and recover things we have experienced or learned in the past. Researchers have classified the memories after many years of research. There is a difference between memory types and stages of memory. Memory can either be implicit or explicit whereas stages of memory are working, short-term, and long-term. Information that humans don’t try to remember on purpose – it is also referred to as unconscious memory, is stored in implicit memory. Information that people try to remember is stored in their explicit memory.

Working memory, information from the world around us, is stored for a short period of time. Short-term memory includes information that people are aware of. Long-term memory includes information outside of the awareness. caused by cerebrovascular accident, tumor, hypoxia, encephalitis, or chronic alcoholism.

People with anterograde amnesia are not able to create new memories from the time of trauma onwards. It can be caused by the effects of long-term alcoholism, head trauma, encephalitis, Wernicke–Korsakoff syndrome and cerebrovascular events or other trauma. The two brain regions involved in this condition are medial diencephalon and medial temporal lobe. Retrograde amnesia is usually temporary. Retrograde amnesia can also result from damage to different regions of the brain. These include the thalamus (deep in the center of the brain) and the hippocampus (temporal lobe).

The patients’ role in investigating memory diseases has been important in medical history. Henry Gustav Molaison (H.M.) is thought to be the best known patient in neuroscience. Patient H.M. suffered from severe seizures. By 1953, he was no longer able to keep his job as a motor winder on an assembly line. Molaison allowed surgeons to remove a small-sized section of tissue from each hemisphere of his brain for the back then treatment of seizures.

After it, he was left with permanent amnesia. He was able to recall memories from his childhood, facts about his parents – but he was no longer able to form new memories. Scoville and Milner’s observations pointed to a specific structure within the medial temporal lobe that was necessary for memory – the hippocampus. Over the next five decades, neuroscientists studying patient H.M. learned about the hippocampus and adjacent regions. Those parts transform the awareness into memories that can be stored for a lifetime.

But what happens when these memories, that build up slowly during your life, begin to disappear? When talking about memory loss, the most widely known, probably the first disease that comes into your mind is Alzheimer’s disease (AD). AD is a progressive neurodegenerative disease that is characterized by the accumulation of Amyloid plaques and neurofibrillary tangles and presents itself with neocortical atrophy. At the moment, it is the most seen cause of dementia, with 30 million people worldwide being affected, and this number is only expected to increase, due to the progressive aging of the population .

There are mainly two causes for AD: sporadic and familial, the latter representing up to 5% of all cases . Although it isn’t a big percentage, it still represents an important subgroup, as it can have the most common early-onset neurodegenerative memory loss. Because it is a very uncommon form of the disease, it is usually underdiagnosed or diagnosed late, with an average of a 1.6-year delay compared with late-onset AD.

Although there isn’t a complete clarity in what causes the disease, studies have demonstrated that they are at least 230 mutations involving the synthesis and proteolysis of beta-amyloid peptide. In about 50% of the patients’ present mutations in PS1 and PS2, as well as in the amyloid precursor protein, there has been stablished a relation between these mutations and an autosomal dominant form of early onset familial Alzheimer’s disease (EOFAD).

AD usually presents itself with learning difficulties and progressive neuron and synaptic loss and it is caused, as said earlier, by amyloid plaques and neurofibrillary tangles composed of hyperphosphorylated aggregates microtubule-associated protein tau. -. Semantic memory is first impaired, usually several years prior to diagnosis, and as the hippocampus damage progresses, it becomes impossible to form new memories.

The atrophy starts in the entorhinal cortex and hippocampal formations, which later spread to other cerebral regions. Poorly myelinated neurons are the first ones to present lesions, and highly myelinated ones are only affected in the final stages of the disease. This atrophy progresses slowly, but while healthy human brains lose about 0.2% of brain volume per year, in AD the rates are ten times faster. Grey matter volume plays an important role in memory too, as left hippocampal gray matter has an important correlation with memory and left temporal grey matter volume is important for language tasks.

AD is not the only memory-related disease caused by the protein tau. Mutations in this protein cause frontotemporal dementia, as it has been discovered that there is an aberrant accumulation of it. This type of dementia presents usually before 65 years of age, like EOFAD, and usually manifest with personality and social behavior changes, with some preservation of memory until the final stages of the disease. The majority of these cases are sporadic, but it has been found that around 3% of all cases are familial, with a similar presentation of the protein as in AD.

Through this essay we have analyzed memory, its different subtypes and first discoveries, and illnesses that may affect it. As the age of the population increases, the memory loss does too. That is the reason why there are a lot of studies focusing on this issue. Some recent and promising clinical trials include vaccination against AD using amyloid-beta antibodies, which has had positive results in animals, if administered over a long period of time and before amyloid plaques appear.

Another study used neural stem cells from fetal brain tissue, and the subjects showed an increase in memory consolidation. Another study conducted on rodents emonstrated that treadmill exercise enhances synaptic plasticity in the hippocampus and pre-frontal cortex, improving significantly its spatial working memory.

Memory is a very promising and powerful field of study, that only continues to grow every day, as the loss of it is becoming one of humanities most urgent concerns.

References

(1) Wikipedia page about learning [10.03.2022], https://en.wikipedia.org/wiki/Learning

(2) Charles Stangor, Jennifer Walinga, Introduction to Psychology – 1st Canadian
Edition, Chapter 9. Remembering and Judging

(3) Richard J. Allen, Classic and recent advances in understanding amnesia

(4) Haist, F., Shimamura, A. P., & Squire, L. R. (1992), On the relationship between recall and recognition memory. Journal of Experimental Psychology: Learning, Memory, and Cognition, Wikipedia page about amnesia https://en.wikipedia.org/wiki/Amnesia

(5) Larry R. Squire, The Legacy of Patient H.M. for Neuroscience, Neuron January 2009

(6) Deborah Halber, The Curious Case of Patient H.M.

(7)Wimo A., Jonsson L., Winblad B. An estimate of the worldwide prevalence and direct costs of dementia in 2003. Dement Geriatr Cogn Dis. 2006;21:175–181

(8) Wu L, Rosa-Neto P, Hsiung GY, Sadovnick AD, Masellis M, Black SE, Jia J, Gauthier S. Early-onset familial Alzheimer's disease (EOFAD). Can J Neurol Sci. 2012 Jul;39(4):436-45. doi: 10.1017/s0317167100013949. PMID: 22728850.

(9) Zhu XC, Tan L, Wang HF, et al. Rate of early onset Alzheimer’s disease: a systematic review and meta-analysis. Ann Translational Med 2015;3(3):38.

(10) van Vliet D, de Vugt ME, Bakker C, et al. Time to diagnosis in young-onset dementia as compared with late-onset dementia. Psychol Med 2013;43(2):423–32.

(11) Lleo A, Blesa R, Queralt R, et al. Frequency of mutations in the presenilin and amyloid precursor protein genes in early-onset Alzheimer disease in Spain. Arch Neurol. 2002;59:1759-63

(12) Walsh DM, Selkoe DJ. Deciphering the molecular basis of memory failure in Alzheimer’s disease. Neuron 2004;44:181–193.

(13) Grundke-Iqbal I, Iqbal K, Tung YC, Quinlan M, Wisniewski HM, Binder LI. Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology. Proc Natl Acad Sci USA 1986;83:4913–4917

(14) Semantic memory and language dysfunction in early Alzheimer's disease: a review.
Verma M, Howard RJ Int J Geriatr Psychiatry. 2012 Dec; 27(12):1209-17.

(15) Clinical dementia rating: a reliable and valid diagnostic and staging measure for dementia of the Alzheimer type. Morris JC Int Psychogeriatr. 1997; 9 Suppl 1():173-6; discussion 177-8.

(16) Development of Alzheimer-related neurofibrillary changes in the neocortex inversely recapitulates cortical myelogenesis. Braak H, Braak E Acta Neuropathol. 1996 Aug; 92(2):197-201.

(17) Vulnerability of select neuronal types to Alzheimer's disease. Braak H, Del Tredici K, Schultz C, Braak E Ann N Y Acad Sci. 2000; 924():53-61.

(18) Visualisation and quantification of rates of atrophy in Alzheimer's disease. Fox NC, Freeborough PA, Rossor MN Lancet. 1996 Jul 13; 348(9020):94-7.

(19) Hernandez F, Avila J. Tauopathies. Cell Mol Life Sci 2007;64:2219–2233

(20) A. Brun, B. Englund, L. Gustafson, U. Passant, D.M.A. Mann, D. Neary, J.S. Snowden, J. Neurol. Neurosurg. Psychiatry 57 (1994) 416^418

(21) M. Stevens, C.M. van Duijn, W. Kamphorst, P. de Knij°, P.Heutink, W.A. van Gool, P. Scheltens, R. Eavid, B.A. Oostra, M.F. Niermeijer, J.C. van Swieten, Neurology 50 (1998)
1541^1545.

(22) Ager, R. R. et al. Human neural stem cells improve cognition and promote synaptic growth in two complementary transgenic models of Alzheimer's disease and neuronal loss. Hippocampus 25, 813–826 (2015).

(23) Mu L, Cai J, Gu B, Yu L, Li C, Liu QS, Zhao L. Treadmill Exercise Prevents Decline in Spatial Learning and Memory in 3×Tg-AD Mice through Enhancement of Structural Synaptic Plasticity of the Hippocampus and Prefrontal Cortex. Cells. 2022 Jan 12;11(2):244. doi: 10.3390/cells11020244. PMID: 35053360; PMCID: PMC8774241.

Author's bio

Amelia Kudasik is a high school student from Poland. She is interested in neuroscience, medicine and global health. She started the BRAIN for STEM project, an international organization bringing together young researchers. She is a volunteer.

Jimena Rodríguez Encinas is a high school student from Madrid, Spain. Since she was a child, Jimena has been dreaming of becoming a doctor, particularly a neurosurgeon. Because of her interest on everything related to the brain, she has taken several neuroscience courses, with the hope to learn more about it.