What is Alzheimer Disease?

Alzheimer Disease
Increased CSPalpha immunostaining in Alzheimer’s disease cerebellum. Fixed cerebellar cortex sections from a patient with severe Alzheimer’s disease (B, D) and a control subject (A, C) were probed with anti-CSPalpha antibodies for analysis of CSPalpha expression. CSPalpha expression in the cerebellar cortex of the Alzheimer’s disease patient appeared higher than in the control subject. In A and B cerebellar cortex with the Purkinje cell layer and granule cells are visible in the lower right corner. There is increased immunoreactivity in the neuropil in Alzheimer’s disease as compared to an age-matched control case. In C and D the granule cells of the cerebellum show increased cytoplasmic and neuropil labeling in Alzheimer’s disease as compared to an age-matched control. Negative control images are shown in E and F (immunohistochemistry with omission of the primary antibody) and confirm the specificity of labeling in Figure 5 and Additional file 1: Figure S1. Haematoxylin counterstaining is also shown. Original magnification: 400×. Scale bars represent 20 μm.Evidence that the presynaptic vesicle protein CSPalpha is a key player in synaptic degeneration and protection in Alzheimer's disease. Tiwari SS, d'Orange M, Troakes C, Shurovi BN, Engmann O, Noble W, Hortobágyi T, Giese KP - Molecular brain (2015). Not Altered. CC.

Alzheimer disease is a neurodegenerative disorder marked by cognitive and behavioral impairment that significantly interferes with social and occupational functioning. It is an incurable disease with a long preclinical period and progressive course. 

What is the Pathology of Alzheimer Disease?

Etiology: The etiology of Alzheimer disease is unknown. 

Genes involved: Amyloid precursor protein (APP) at chromosome 21, presenilin (PS) 1 and 2 (chromosome 14 and 1), and the gene encoding apolipoprotein E (ApoE) linked to chromosome 19 is a risk factor for late-onset AD.

Pathogenesis: The sequence of events that lead to Alzheimer disease is the alteration in one or more aspects of beta amyloid, leading to proliferation of extracellular amyloid plaques. Another pathway involves alteration in one or more aspects of tau protein metabolism, leading to intracellular neurofibrillary tangles. As part of these processes, an inflammatory cascade causes oxidative neuronal injuries and depletion of several neurotransmitters.

Histology: The histology associated with Alzheimer disease shows extracellular amorphus eosinophilic deposits of amyloid consisting of Aβ peptides, which are referred to as amyloid plaques and neurofibrillary tangles which are intraneuronal aggregates of abnormally modified microtubule-associated protein tau.

How does Alzheimer Disease Present?

Patients with Alzheimer disease typically are older. It has a higher occurrence in women. The symptoms, features, and clinical findings associated with Alzheimer disease include memory loss, poor judgment, and mood changes. 

How is Alzheimer Disease Diagnosed?

Alzheimer disease is diagnosed by clinical and physical exam. 

How is Alzheimer Disease Treated?

Alzheimer disease has no cure. Some medications may help with symptoms such as Acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine). Other treatments include cognative rehabilitation and cognitive stimulation. 

What is the Prognosis of Alzheimer disease?

The prognosis of Alzheimer disease fair. 

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Last updated on May 26, 2022