Demensia Aspek neuropatobiologis



Aswin Soedjono(1*)

(1) LaboratoriumNeuropsikobiologi BagianAnatomi, Embriologi &Antropologi Fakultas Kedokteran, Universitas GadjahMada Yogyakarta
(*) Corresponding Author

Abstract


Dementia is a complex clinical syndrome resulting fromdysfunction ofmultiple brain systems caused by heterogeneousmechanisms,
ranging from the toxic effect of drugs to infection, genetic, ischemia, hormonal imbalances,
systemic pathologies and specific brain diseases, characterized by peculiar pathologic changes, for
instance the abnormal deposition of hyperphosphorylated tau protein or -synuclein. Themain clinical categories
are: i. cognitive impairment; ii. behavioral and psychological symptoms; iii. physical andmotor symptoms. In turn,
all of them affect both quality of life and activity of daily living. Dementia, as a neurobehavioral syndrome,
consists of symptoms collectively called disorder of global cognitive power, which is not followed by deterioration
the degree of alertness, but related to behavioral changes.Despite of the complexity of deseases underlying
dementia, the understanding of neuropathobiological perspectives of dementia is a very usefulmeans in the
effort to elucidate themechanisms, diagnosis, andmanagement of dementia in general.The brains ofAlzheimer’s
disease patients exhibit a variety of degenerative changes, including the loss of dendrites and synapses, neuron
death, abnormal capillaries, senile plaques, and neurofibrillary tangles.Cognitive symptoms, ie.memory deficit,
involves hippocampus and entorhinal area.Dysfunction of associative neocortex results fromits disconnection
fromthemesial temporal lobe.Disconnection of dorsolateral prefrontal cortex leads to deficit of both episodic and
workingmemory. Temporal-parietal disconnection has been associatedwith other cognitive disturbances, such
as apraxia and agnosia.Behavioral and psychological symptoms, such as apathy and depression are thought to
derive fromdysfunction of the fronal lobe and anterior limbic system.Physical andmotor symptoms (tremor, axial
rigidity and bradykinesia) can complicatedAlzheimer’s disease in the advanced stage due to the spreading of
pathological change to cortical and deep motor structures. The present paper discusses some principles of
neuropathobiological aspects (neuroanatomy, neurophysiology, neuropsychology, and neuropathology) involved
in dementia.





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