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Advanced Neurology Dementia with Lewy bodies and substance misuse

A B C D

Figure 2. Comparison of clock drawing task results. The subject was asked to draw a clock with the hand pointing to ten past eleven as part of the Montreal
Cognitive Assessments evaluation. (A) February 2018: 18/30; (B) May 2018: 20/30; (C) March 2019: 18/30; (D) July 2019: 15/30.

Figure 3. Clinical timeline and history from when the patient first began seeking treatment in 2012 to his diagnosis in 2017 and death in late 2021. Different
diagnoses given as well as symptoms suggestive of dementia with Lewy bodies are in bold.

manifestations such as neurofibrillary tangles and plaques, recruited to and congregate at the site of cellular damage.
and abnormal accumulations of protein, predominantly Although α-synuclein and β-amyloid are meant to repair
tau and β-amyloid. 51-53 damage, proteasome degradation may result in increased
α-synuclein and β-amyloid are proteins that are aggregation. 65-69 Neuroinflammation increases the release
found in healthy individuals and are vital for normal of calcium-dependent calpain proteases, which cleave the
brain functioning. α-synuclein is normally involved in α-synuclein in ways that are more likely to encourage their
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the repair of damaged DNA as a DNA-binding protein, aggregation. Calcium also induces increased aggregation
synaptic vesicle trafficking, and neurotransmitter directly by encouraging the α-synuclein to cluster. 65,66,71,72
release. 55-62 It is predisposed to aggregation, as this helps Chronic damage results in increased DNA mutations
concentrate the neurotransmitters for release. 58,63 One of in the proteins and oxidative stress interferes with the
the functions of β-amyloid is thought to be the prevention folding process, causing the proteins to form abnormal
of cell death from oxidative damage. These proteins are clumps. Neuroinflammation damages astrocytes and
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Volume 3 Issue 1 (2024) 6 https://doi.org/10.36922/an.2232