Synaptic retrogenesis and amyloid-beta in Alzheimer's disease.

• Pathological hallmarks of Alzheimer's disease (AD) include synaptic and neuronal degeneration and the presence of extracellular deposits of amyloid-beta (Abeta) in senile plaques in the cerebral cortex. Although these brain lesions may be seen also in aged non-demented individuals, the increase in brain Abeta is believed by many to represent the earliest event in the disease process. Accumulating evidence suggests that Abeta, which is highly conserved by evolution, may have an important physiological role in synapse elimination during brain development. An intriguing idea is that this putative function can become pathogenic if activated in the aging brain. Here, we review the literature on the possible physiological roles of Abeta and its precursor protein AbetaPP during development with special focus on electrophysiological findings.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Psykiatri (hsv//swe)

MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Psychiatry (hsv//eng)

Nyckelord

Alzheimer Disease

metabolism

pathology

Amyloid beta-Protein

metabolism

physiology

toxicity

Amyloid beta-Protein Precursor

metabolism

physiology

Animals

Brain

growth & development

Cell Proliferation

Glutamic Acid

physiology

Humans

Long-Term Potentiation

physiology

Memory

physiology

Neuronal Plasticity

physiology

Synapses

pathology

physiology

Publikations- och innehållstyp

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