It was an overcast Saturday on June 15, 1968. The music stopped strumming from a virtuoso known for superimposing triads and arpeggios without the use of a guitar pick. Wes Montgomery died of a heart attack at the age of 45.  Your bowl of cereal went soggy during a contemplative pause after hearing the news.
You’re planning a wedding. Someone suggests, June 15th and your mind associates the melancholy date. Perhaps a week earlier or later? It makes no difference, because with hyperthymesia you remember every event of every day. On each, there is both good and bad news.
The bully who taunted you in grade school; the teacher that praised you for straight receiving straight A’s. Past loves and breakups are all preserved as virtual high-definition recordings in your brain.
Among less than 100 people with highly superior autobiographical memory (HSAM) called hyperthymesia, you won’t have those “senior moments” of agitation from forgetting trivia that relates to personal life. Three years before the death of that favorite jazz musician, Wes Montgomery received two Grammy Award nominations for Bumpin’ played on the Gibson L-5 acoustic guitar.
Autobiographical memory is an important distinction. Because it seems that those with hyperthymesia remember personal life events in extraordinary detail. But they are no better than the average person at recalling impersonal information, such as random lists of words. 
Human memory is an intangible mystery of recall that attracts interests of philosophers, scientists, and people in general. Recent intellectual, cognitive, and neuroimaging studies lead to speculation that the amygdala likely supports the encoding and retrieval of autobiographical memory. 
Swinging to the opposite realm of unforgettable memories leads you to an insidious disease called Alzheimer’s. This and other forms of dementia occur within individuals with an overproduction of cholinesterase. This protein breaks down acetylcholine, a neurotransmitter responsible for modulating memory, muscle movement, and motivation. An overabundance of cholinesterase causes the beta amyloid to form blockages, degrading neuron activity.
Groups of neuroscientists studying the genetics of the condition have discovered that hyperthymesia develops due to an allele known as apolipoprotein E2 (APOE2), an allele of the APOE gene that has a positive correlation with improved working memory capacity and is a counterpart to APOE4. Thus, through additional neurology research, the uncommon condition of hyperthymesia may lead to gene therapy for patients with dementia. 
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