Postsynaptic density protein: Difference between revisions

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== Disease ==

There are more than 130 diseases are attributed to changes in the proteome of excitatory synapses. Given that PSD-95 belongs to the proteome of excitatory synapses, research has found that any mutations with PSD-95 caused complications not only for how quickly synapses transmitted neurotransmitters but its capability to conform to new stresses. Therefore, since PSD-95 is integral for synaptic stability, a decrease in PSD-95 has substantial neurological effects based on age and the area of the brain affected.

1. Media Prefrontal Cortex - Under normal circumstances, PSD-95 continues to increase from birth until peaking during adolescents. However, if the PSD-95 is decreased, it will affect the medial prefrontal cortex (mPFC) which is responsible for cognition, working memory, and sociability (Coley, 2019). Researchers found that the PSD-95 knockout mice lacked sociability and exhibited both learning and working memory deficiencies. The dysfunction of PSD-95 is believed to manifest to some degree in humans as either schizophrenia or as autism (Coley, 2019). It has also been linked to Alzheimer’s by a research study.

2. Superior Temporal Sulcus - This research study focused on the superior temporal sulcus. The disease is mainly characterized by neuronal damage, neuronal death, and brain atrophy. The study found that in a group of post-mortem subjects; demented subjects had 50% less PSD-95 concentration than the control group (Perez-Nievas, 2013). This was compared to a group that had many of the same morphological signs as those with Alzheimer’s but suffered no adverse effects from it. This group had significantly more PSD-95 than a normal brain, perhaps to counter act the degrading aspects.

1.Media Prefrontal Cortex - Under normal circumstances, PSD-95 continues to increase from birth until peaking during adolescents. However, if the PSD-95 is decreased, it will affect the medial prefrontal cortex (mPFC) which is responsible for cognition, working memory, and sociability (Coley, 2019). Researchers found that the PSD-95 knockout mice lacked sociability and exhibited both learning and working memory deficiencies. The dysfunction of PSD-95 is believed to manifest to some degree in humans as either schizophrenia or as autism (Coley, 2019). It has also been linked to Alzheimer’s by a research study.

3. Corpus Striatum – A study of cocaine abuse using a mice study suggests that psychostimulants decrease the PSD-95 levels in both the dorsal and ventral portions of the striatum though the hippocampus and cortex were unaffected. While less than 2 injections made little change in PSD-95 levels, 3 to 10 injections resulted in substantial chronic PSD-95 loss; however, 11 or more injections showed no additional decreases (Yao et al., 2004). When studied months after the last injection, the deficits in PSD-95 remained, suggesting long-term neuronal effects of drug use.

2.Superior Temporal Sulcus - This research study focused on the superior temporal sulcus. The disease is mainly characterized by neuronal damage, neuronal death, and brain atrophy. The study found that in a group of post-mortem subjects; demented subjects had 50% less PSD-95 concentration than the control group (Perez-Nievas, 2013). This was compared to a group that had many of the same morphological signs as those with Alzheimer’s but suffered no adverse effects from it. This group had significantly more PSD-95 than a normal brain, perhaps to counter act the degrading aspects.

3.Corpus Striatum – A study of cocaine abuse using a mice study suggests that psychostimulants decrease the PSD-95 levels in both the dorsal and ventral portions of the striatum though the hippocampus and cortex were unaffected. While less than 2 injections made little change in PSD-95 levels, 3 to 10 injections resulted in substantial chronic PSD-95 loss; however, 11 or more injections showed no additional decreases (Yao et al., 2004). When studied months after the last injection, the deficits in PSD-95 remained, suggesting long-term neuronal effects of drug use.

== Relevance ==

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 == Disease ==
 There are more than 130 diseases are attributed to changes in the proteome of excitatory synapses. Given that PSD-95 belongs to the proteome of excitatory synapses, research has found that any mutations with PSD-95 caused complications not only for how quickly synapses transmitted neurotransmitters but its capability to conform to new stresses. Therefore, since PSD-95 is integral for synaptic stability, a decrease in PSD-95 has substantial neurological effects based on age and the area of the brain affected.
-.	Media Prefrontal Cortex - Under normal circumstances, PSD-95 continues to increase from birth until peaking during adolescents. However, if the PSD-95 is decreased, it will affect the medial prefrontal cortex (mPFC) which is responsible for cognition, working memory, and sociability (Coley, 2019). Researchers found that the PSD-95 knockout mice lacked sociability and exhibited both learning and working memory deficiencies. The dysfunction of PSD-95 is believed to manifest to some degree in humans as either schizophrenia or as autism (Coley, 2019). It has also been linked to Alzheimer’s by a research study.
-.	Superior Temporal Sulcus - This research study focused on the superior temporal sulcus. The disease is mainly characterized by neuronal damage, neuronal death, and brain atrophy. The study found that in a group of post-mortem subjects; demented subjects had 50% less PSD-95 concentration than the control group (Perez-Nievas, 2013). This was compared to a group that had many of the same morphological signs as those with Alzheimer’s but suffered no adverse effects from it. This group had significantly more PSD-95 than a normal brain, perhaps to counter act the degrading aspects.
+.Media Prefrontal Cortex - Under normal circumstances, PSD-95 continues to increase from birth until peaking during adolescents. However, if the PSD-95 is decreased, it will affect the medial prefrontal cortex (mPFC) which is responsible for cognition, working memory, and sociability (Coley, 2019). Researchers found that the PSD-95 knockout mice lacked sociability and exhibited both learning and working memory deficiencies. The dysfunction of PSD-95 is believed to manifest to some degree in humans as either schizophrenia or as autism (Coley, 2019). It has also been linked to Alzheimer’s by a research study.
-.	Corpus Striatum – A study of cocaine abuse using a mice study suggests that psychostimulants decrease the PSD-95 levels in both the dorsal and ventral portions of the striatum though the hippocampus and cortex were unaffected. While less than 2 injections made little change in PSD-95 levels, 3 to 10 injections resulted in substantial chronic PSD-95 loss; however, 11 or more injections showed no additional decreases (Yao et al., 2004). When studied months after the last injection, the deficits in PSD-95 remained, suggesting long-term neuronal effects of drug use.
+.Superior Temporal Sulcus - This research study focused on the superior temporal sulcus. The disease is mainly characterized by neuronal damage, neuronal death, and brain atrophy. The study found that in a group of post-mortem subjects; demented subjects had 50% less PSD-95 concentration than the control group (Perez-Nievas, 2013). This was compared to a group that had many of the same morphological signs as those with Alzheimer’s but suffered no adverse effects from it. This group had significantly more PSD-95 than a normal brain, perhaps to counter act the degrading aspects.
+.Corpus Striatum – A study of cocaine abuse using a mice study suggests that psychostimulants decrease the PSD-95 levels in both the dorsal and ventral portions of the striatum though the hippocampus and cortex were unaffected. While less than 2 injections made little change in PSD-95 levels, 3 to 10 injections resulted in substantial chronic PSD-95 loss; however, 11 or more injections showed no additional decreases (Yao et al., 2004). When studied months after the last injection, the deficits in PSD-95 remained, suggesting long-term neuronal effects of drug use.
 == Relevance ==