Cognitive Deficits in Neurodegenerative Disorders: Parkinson’s Disease and Alzheimer’s Disease

Chapter
Part of the Advances in Neurobiology book series (NEUROBIOL, volume 1)

Abstract

Among the most important neurodegenerative disorders affecting aging adults around the world are Alzheimer’s disease (AD), which affects around 4.5 million people in the United States, and Parkinson’s disease (PD), which has a prevalence of about 160 cases per 100,000 people and an incidence of about 20 cases per 100,000 people per year. In both disorders prevalence and incidence increase with age. AD is the main dementing disorder, whereas cognitive dysfunction and dementia eventually occur in 20–40% of patients with PD. In this chapter the neurobiology of these diseases is reviewed. Classical, anatomically defined local circuits are summarized. Data obtained using advanced imaging techniques, such as SPECT, and functional MRI, and electrophysiological recordings, are highlighted. The main emphasis for both PD and AD is on cognitive deficits from the perspective of brain circuits and synaptic physiological abnormalities as well as on their biochemical correlates. In particular, among nonmotor defects in Parkinson’s disease sensory deficits are also emphasized in relation to visuocogntive and attentive dysfunction. The main neurotransmitter systems involved are dopamine (in PD) and acetylcholine (both in PD and AD). The logic role of dopamine in the retinal circuitry is discussed in relation to sensory (visual) dysfunction in PD. The contribution of neurotransmitter/modulators beyond the dopaminergic and cholinergic systems in the basal ganglia and in several cortical areas is reviewed. This involves glutamate, adenosine, and GABA. The cognitive effect of genetic variability of catechol-o-methyltranferase, in the prefrontal cortex is summarized. Although advances in the understanding of AD and PD pathophysiology have been significant, fundamental issues remain unsolved. The powerful neuropathological arguments concerning the progression of PD based on alpha synuclein predict late involvement of cortical circuits, presumably responsible for cognitive changes. The role of acetylcholine and diverse cholinergic receptors in cognitive dysfunction in both AD and PD will need further studies. Future studies may potentially lead to a bridging theory of cognitive impairment in both AD and PD.

Keywords

Dopamine Basal ganglia Frontal cortex Striatum Vision D1 and D2 dopamine receptors Retina Visual cognition GABA Subthalamic nucleus Cholinergic mechanisms Glutamate Adenosine Thalamocortical processing Alzheimer’s disease (AD) Mild cognitive impairment (MCI) Amyloid precursor protein (APP) Amyloid beta (Aβ) tau Apolipoprotein E ɛ4 (APOE4) Cerebral blood volume (CBV) Positron emission tomography (PET) Magnetic resonance imaging (MRI) 

Notes

Acknowledgments

I thank Yafell Serulle and Michaelangelo Fuortes for critical reading of the manuscript and Sergio Angulo for assistance with graphics design. HM was supported by NIH grant AG27476.

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© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.Department of NeurologySUNY Downstate Medical CenterBrooklynUSA
  2. 2.Department of OphthalmologySUNY Downstate Medical CenterBrooklynUSA
  3. 3.Division of Movement Disorders, Department of NeurologyParkinson’s Disease and Related Disorders Clinic, Center of Excellence NPFBrooklynUSA
  4. 4.Department of Neurology and Physiology/PharmacologySUNY Downstate Medical CenterBrooklynUSA

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